Optic neuropathy associated with the use of over-the-counter sexual enhancement supplements.
ABSTRACT: This case report details an association of the use of over-the-counter sexual enhancement supplements with atypical optic neuropathy. A 42-year-old man presented with right-sided headache and vision loss of the right eye, which deteriorated to a single quadrant of hand motion over 11 days. Serial orbital magnetic resonance imaging scans demonstrated progressive orbital optic nerve enhancement extending into the optic canal despite high-dose steroid treatment. The patient eventually admitted to using several over-the-counter sexual enhancement supplements prior to the onset of symptoms and throughout the course of his steroid treatment, which he subsequently discontinued. His vision improved to 20/200 with an expanded visual field. Anterior ischemic optic neuropathy has been reported in association with phosphodiesterase (PDE)-5 inhibitor use, but visual loss in association with unregulated sexual enhancement supplements has not been studied. While one case cannot establish association, our case is suggestive of potential dangers of over-the-counter sexual enhancement supplements, which may contain PDE-5 inhibitors, "male hormones," and "substances that enhance blood production." The case also underscores the importance of obtaining a careful history of supplements in patients with optic neuropathies.
Project description:BACKGROUND:Orbital cellulitis is an ophthalmic emergency, which is associated with vision-threatening adverse effects. The purpose of this study is investigating etiology, radiologic findings, management and complications of patients with non-medial orbital cellulitis. METHOD:A retrospective medical record and radiologic file review of patients with infectious orbital cellulitis was performed to detect all patients with non-medial orbital cellulitis who referred to Khalili hospital from 2016 to 2019. Age, sex, origin of infection, size of collection or abscess, medical or surgical management, microbiology, first and final best-corrected visual acuity, duration of admission, and complications was recorded. Patients divided into two groups; medical management and surgical management groups and all of data compared between in this groups. RESULTS:Of ninety-six patients with infectious orbital cellulitis, 23 cases (14 male, 9 female) were included. Five patients (21.7%) were managed medically and 18 patients (78.3%) were managed surgically. Patients' age range was 5-70?years old. Most common location for non-medial cellulitis was superior space (66.7% in surgical and 40% in medical group; p?=?0.511). In 13 cases of surgical group (72.3%) were detected microorganisms. The mean?±?SD of collection volume in medical group were 476.5?±?290.93?mm3 and 2572.94?±?1075.75?mm3 in surgical group (p?<?0.001). Ten patients in surgical group had compressive optic neuropathy. The mean?±?SD of collection volume was 3204.97?±?879.88?mm3 in patient with compressive optic neuropathy and 1280.43?±?880.68?mm3 in patient without compressive optic neuropathy (P?<?0.001). One case complicated by subdural empyema and another case progressed to necrotizing fasciitis. CONCLUSION:Non-medial orbital cellulitis is an uncommon but sight-threatening and life-threatening condition. Timely diagnosis and accurate management reduce morbidity and mortality. Combined surgery for patients with superior or supra-temporal and large non-medial abscess is recommended.
Project description:There are various causes that can lead to compressive optic neuropathy. We present here orbital apex cyst as an unusual cause of compressive optic neuropathy in a 49-year-old male. He presented with 2 weeks painless loss of vision in the left eye with left-sided headache. He had had left functional endoscopic sinus surgery for left nasal polyps 4 years earlier. Magnetic resonance imaging of brain and orbit revealed a left discrete orbital nodule, possibly orbital cyst or mucocele, which was compressing on the left optic nerve. Left eye vision improved markedly from hand movement to 6/36 pinhole 6/18 after initiation of intravenous dexamethasone. A subsequent endoscopic endonasal left optic nerve decompression found the orbital nodule lesion to be an orbital cyst. Marsupialization was performed instead of excision, as the cyst ruptured intraoperatively. Postoperative vision improved to 6/7.5 with normal optic nerve function postoperatively. Possible cause of orbital apex cyst is discussed.
Project description:PURPOSE:To evaluate the effectiveness of steroid-pulse therapy and three-wall orbital decompression in patients with dysthyroid optic neuropathy (DON). METHODS:Twenty-five patients (46 eyes) with a diagnosis of DON between 2008 and 2015 were included in the study. The first group (7 patients, 16 eyes) consisted of patients with a steroid-pulse treatment only and the second group (18 patients, 30 eyes) included patients with medical and surgical decompression. RESULTS:Twenty patients were female; five patients were male. After the diagnosis of DON, all patients were treated with steroid-pulse treatment (intravenous 500?mg prednisolon twice/week for 4 weeks, 250?mg twice/week for 2 weeks) as a first-line treatment (medical decompression). In 30 eyes (18 patients) out of 46 eyes, (25 patients) an orbital decompression was needed to preserve the optic nerve function. In those therapy-resistant cases (surgical decompression group), the orbital decompression led to statistically significant improvements in best-corrected visual acuity (BCVA), protan and tritan value of the color vision (p?=?0.007, p?<?0.0001, p?=?0.019, respectively, comparison of first visit to last visit). CONCLUSION:According to our data, the mild cases of DON with better initial visual acuity (in our case series mean: 0.3 logMAR) seem to respond well to steroid treatment. However, therapy-resistant cases with an impaired initial BCVA (in our case series, mean: 0.6 logMAR) seem to need the surgery to preserve the optic nerve function. In conclusion, this retrospective study confirms the effectiveness of surgical decompression in therapy-resistant cases of DON.
Project description:Purpose. To describe a patient who developed bilateral, simultaneous nonarteritic anterior ischemic optic neuropathy (NAION) after ingestion of Sildenafil citrate (Viagra) for erectile dysfunction. Methods. Observational case report. Results. A 60-year-old diabetic man noted sudden decrease of vision in both eyes 16 hours after his third consecutive 50?mg daily Sildenafil ingestion. A diagnosis of bilateral NAION was made and he was treated for three days with methylprednisolone 1 g/d intravenously, followed by oral prednisone 75?mg/d. Final visual acuity was 20/50 right eye (OD) and 20/20 left eye (OS). He had preexisting diabetes. Conclusion. This is the first reported case of simultaneous bilateral NAION occurred in a diabetic patient early after Sildenafil intake. Patients with predisposing conditions such as diabetes have to be warned against the use of PDE inhibitors.
Project description:Leber's hereditary optic neuropathy (LHON) associated with mutations in mitochondrial DNA (mtDNA) typically manifests only optic nerve involvement but in some patients may develop additional neurological complications. The cause of this association is not clear.We present a case of a 24-year-old male with a history of subacute, painless, and rapidly progressive bilateral vision loss. We performed ophthalmological, neurological and neuropsychological investigations in the proband and his LHON family. The proband showed optic neuropathy, epilepsy, migraine, and intellectual disability; all the maternal relatives did not manifest optic neuropathy but a moderate to severe intellectual disability. Genetic screening revealed a novel association of the LHON m.3460G?>?A primary mutation with the m.T961delT?+?C(n)ins within the mitochondrial encoded 12S RNA (MTRNR1) gene which segregates with the intellectual disability through the maternal branch of the family. We also found a significant increase of mtDNA content in all the unaffected homo/heteroplasmic mutation carriers with respect to either affected or control subjects.This is the first case reporting the co-segregation of a mutation in MTRNR1 gene with a LHON primary mutation, which may be a risk factor of the extraocular signs complicating LHON phenotype. In addition, the data herein reported, confirmed that the key factor modulating the penetrance of optic atrophy in the family is the amount of mtDNA.
Project description:Orbital decompression is a surgical procedure aimed at increasing the orbital volume and/or decreasing the volume of the orbital fat. The indications for orbital decompression are determined in the course of thorough eye examination. An important objective of examination of a patient with thyroid eye disease (TED) is determination of inflammation activity and severity. Orbital decompression is a surgical procedure that can be performed in both the active and nonactive stages of the disease. However, the indications for the surgery in these cases are different. Optic neuropathy and severe corneal disease are threatening complications that may lead to permanent visual loss and generally occur in the presence of active orbital inflammation. If treatment with high-dose corticosteroids has proven ineffective, an urgent surgical procedure consisting of orbital decompression and, in case of involvement of the cornea, eyelid and corneal surgery has to be performed. Owing to significant progress in technology, improvement of methods and accumulated experience over the past decade, the indications for bone orbital decompression have extended compared to the time when this procedure was used only in patients with extremely severe TED. The most common complication of the orbital decompression is the development or deterioration of previously existing binocular diplopia and strabismus. In addition, other parameters may change as well, including the position of the globe, the eyelids, the angle of deviation of the eye, and intraocular pressure. Thus, bone orbital decompression is a major step of a comprehensive, often multistage, system of rehabilitation of patients with severe refractory TED.
Project description:Purpose:The effective management of glaucoma is hindered by an incomplete understanding of its pathologic mechanism. While important, intraocular pressure (IOP) alone is inadequate in explaining glaucoma. Non-IOP-mediated risk factors such as cerebrospinal fluid (CSF) pressure have been reported to contribute to glaucomatous optic neuropathy. Due to the difficulty associated with experimental measurement of the salient variables, such as the retrobulbar CSF pressure, porosity of the subarachnoid space (SAS), and especially those concerned with the perioptic SAS, there remains a limited understanding of the CSF behavior contributing to the translaminar pressure gradient (TLPG), hypothesized to be a critical factor in the development of glaucoma. Method:An integrated compartmental model describing the intracranial and orbital CSF dynamics, coupled with intraocular dynamics, is developed based on first principles of fluid mechanics. A sensitivity analysis is performed to identify anatomic characteristics that significantly affect the retrobulbar subarachnoid space (RSAS) pressure and, consequently, the TLPG. Results:Of the 28 parameters considered, the RSAS pressure is most sensitive to CSF flow resistance in the optic nerve SAS and the potential lymphatic outflow from the optic nerve SAS into the orbital space. A parametric study demonstrates that a combination of resistance in the range of 1.600 × 1012 - 1.930 × 1012 Pa s/m3 (200.0 - 241.3 mm Hg min/mL) with 5% to 10% lymphatic CSF outflow yields RSAS pressures that are consistent with the limited number of studies in the literature. Conclusions:The results suggest that a small percentage of lymphatic CSF outflow through the optic nerve SAS is likely. In addition, flow resistance in the orbital CSF space, hypothesized to be a function of patient-specific optic nerve SAS architecture and optic canal geometry, is a critical parameter in regulating the RSAS pressure and TLPG.
Project description:Leber Hereditary Optic Neuropathy is an inherited optic neuropathy caused by mitochondrial DNA point mutations leading to sudden, painless loss of vision. We report a case of an 8-year-old boy presenting with a radiological phenotype of longitudinally extensive transverse myelitis on a background of severe visual impairment secondary to Leber Hereditary Optic Neuropathy (LHON). He was found to have dual mitochondrial DNA mutations at 14484 (MTND6 gene) and 4160 (MTND1 gene) in a family with a severe form of LHON characterised by not only an unusually high penetrance of optic neuropathy, but also severe extra-ocular neurological complications. The m.14484T>C mutation is a common LHON mutation, but the m.4160T>C mutation is to our knowledge not reported outside this family and appears to drive the neurological manifestations. To our knowledge there have been no previous reports of spinal cord lesions in children with LHON.
Project description:The nitric oxide - guanylyl cyclase-1 - cyclic guanylate monophosphate (NO-GC-1-cGMP) pathway has emerged as a potential pathogenic mechanism for glaucoma, a common intraocular pressure (IOP)-related optic neuropathy characterized by the degeneration of retinal ganglion cells (RGCs) and their axons in the optic nerve. NO activates GC-1 to increase cGMP levels, which are lowered by cGMP-specific phosphodiesterase (PDE) activity. This pathway appears to play a role in both the regulation of IOP, where reduced cGMP levels in mice leads to elevated IOP and subsequent RGC degeneration. Here, we investigated whether potentiation of cGMP signaling could protect RGCs from glaucomatous degeneration. We administered the PDE5 inhibitor tadalafil orally (10?mg/kg/day) in murine models of two forms of glaucoma - primary open angle glaucoma (POAG; GC-1-/- mice) and primary angle-closure glaucoma (PACG; Microbead Occlusion Model) - and measured RGC viability at both the soma and axon level. To determine the direct effect of increased cGMP on RGCs in vitro, we treated axotomized whole retina and primary RGC cultures with the cGMP analogue 8-Br-cGMP. Tadalafil treatment increased plasma cGMP levels in both models, but did not alter IOP or mean arterial pressure. Nonetheless, tadalafil treatment prevented degeneration of RGC soma and axons in both disease models. Treatment of whole, axotomized retina and primary RGC cultures with 8-Br-cGMP markedly attenuated both necrotic and apoptotic cell death pathways in RGCs. Our findings suggest that enhancement of the NO-GC-1-cGMP pathway protects the RGC body and axon in murine models of POAG and PACG, and that enhanced signaling through this pathway may serve as a novel glaucoma treatment, acting independently of IOP.
Project description:BACKGROUND:During the first few trials of gene therapy for Leber's hereditary optic neuropathy performed by our group, the visual acuity of the patients increased gradually over several months, or even years. However, in the current round of gene therapy for Leber's hereditary optic neuropathy, we noted that the visual acuity of three patients increased rapidly, within a few days after treatment. CASE PRESENTATION:Three patients who were diagnosed with mitochondrial gene 11778 mutation (associated with a G-to-A transition at Mt-11778 in the ND4 subunit gene of complex I of mitochondrial DNA that changes an arginine to histidine at amino acid 340) by genetic diagnosis were followed up three times before gene therapy, which lasted for 1 year, without spontaneous improvement of vision. Visual acuity in one or both eyes of each of the three patients increased rapidly after the initial gene therapy treatment. CONCLUSION:We suspect that in some patients with Leber's hereditary optic neuropathy, a portion of the retinal ganglion cells might remain in a "dormant" state for a certain period of time; these may be activated, within an optimal timeframe, during gene therapy for Leber's hereditary optic neuropathy.