Improving quality of life in patients with end-stage age-related macular degeneration: focus on miniature ocular implants

Low vision devices in the past have been mainly extraocular. There are now four new devices in different stages of development and implementation that are currently available. Three of them, the Implantable Miniature Telescope (IMT, VisionCare Ophthalmic Technologies, Saratoga, CA), Intraocular Lens for Visually Impaired People (IOL-VIP, IOL-VIP System, Soleko, Pontecorvo, Italy), and Lipschitz Mirror Implant (LMI, Optolight Vision Technology, Herzlia, Israel) are implanted into the anterior segment while the Argus II (Second Sight Medical Products, Sylmar, CA) is implanted into the posterior segment. The goal of these devices is to increase the patient quality of life which has been measured by Visual Functioning Questionnaire (VFQ) scales. The IMT is the only device that has been shown to increase the VFQ score by seven points at 6 months compared to baseline. It is the only FDA-approved device in the US while the Argus has been approved in Europe. Each of these prosthetics has potential benefits for patients

Retinal Ganglion Cell Injury Precedes RNFL Loss In Acute Optic Neuritis

Studies in the experimental autoimmune encephalomyelitis (EAE) animal model of MS have shown that RGC injury is an early event in the neurodegeneration of EAE and occurs before transection of axons. Here we tested for RGC injury in patients with acute ON using pattern electroretinogram (PERG) and ganglion cell layer analysis (GCL)

Cavernous Sinus Syndrome: Where Do You Go From Here?

It is well recognized that squamous cell carcinoma of the skin can go on to perineural invasion of the surrounding tissue. However, this diagnosis can be quite challenging in the face as the carcinoma can spread along branches of the trigeminal nerve to invade the cavernous sinus

Retinal Ganglion Cell Injury Precedes RNFL Loss In Acute Optic Neuritis

Studies in the experimental autoimmune encephalomyelitis (EAE) animal model of MS have shown that RGC injury is an early event in the neurodegeneration of EAE and occurs before transection of axons. Here we tested for RGC injury in patients with acute ON using pattern electroretinogram (PERG) and ganglion cell layer analysis (GCL)

Growing Suspicion

loss in the right eye for 3 months. On presentation, vision was 4/200 in the right and 20/20 in the left with an afferent pupillary defect on the right. His visual field was full to confrontation but automated perimetry revealed a central scotoma. The remainder of the exam was normal with the exception of slight elevation of the optic nerve head along with mild perivascular sheathing. He received IV solumedrol for 3 days followed by an oral steroid taper. Fat saturated MRI did not show enhancement of the optic nerve nor any brain abnormalities or mass lesions. He had a normal lab workup including CBC, BMP, quantiferon gold, B12, RPR, and ACE and a normal CXR. On follow up one month later, he experienced no vision improvement. At this point, testing for Leber's hereditary optic neuropathy (LHON) was performed and was negative. He returned 6 months later with subjective worsening of vision in the right eye, however acuity was stable at 4/200. He was started on IVIg therapy and autoimmune and NMO antibodies were drawn. Antibody testing was negative and on follow up one month later, his acuity remained unchanged and his scotoma was larger and denser. He was again lost to follow up for 3 years until he began losing vision in the left eye. Exam revealed counting fingers vision in the right eye and 20/40 with a temporal visual field defect in the left eye. MRI showed an enhancing mass extending from the planum tuberculum and suprasellar area to the right temporal lobe and into both orbits. A procedure was performed

Growing Suspicion

loss in the right eye for 3 months. On presentation, vision was 4/200 in the right and 20/20 in the left with an afferent pupillary defect on the right. His visual field was full to confrontation but automated perimetry revealed a central scotoma. The remainder of the exam was normal with the exception of slight elevation of the optic nerve head along with mild perivascular sheathing. He received IV solumedrol for 3 days followed by an oral steroid taper. Fat saturated MRI did not show enhancement of the optic nerve nor any brain abnormalities or mass lesions. He had a normal lab workup including CBC, BMP, quantiferon gold, B12, RPR, and ACE and a normal CXR. On follow up one month later, he experienced no vision improvement. At this point, testing for Leber's hereditary optic neuropathy (LHON) was performed and was negative. He returned 6 months later with subjective worsening of vision in the right eye, however acuity was stable at 4/200. He was started on IVIg therapy and autoimmune and NMO antibodies were drawn. Antibody testing was negative and on follow up one month later, his acuity remained unchanged and his scotoma was larger and denser. He was again lost to follow up for 3 years until he began losing vision in the left eye. Exam revealed counting fingers vision in the right eye and 20/40 with a temporal visual field defect in the left eye. MRI showed an enhancing mass extending from the planum tuberculum and suprasellar area to the right temporal lobe and into both orbits. A procedure was performed

Growing Suspicion

A 44 year-old man presented to the emergency department in July 2011 for progressive painless visionloss in the right eye for 3 months. On presentation, vision was 4/200 in the right and 20/20 in the leftwith an afferent pupillary defect on the right. His visual field was full to confrontation but automatedperimetry revealed a central scotoma. The remainder of the exam was normal with the exception ofslight elevation of the optic nerve head along with mild perivascular sheathing. He received IVsolumedrol for 3 days followed by an oral steroid taper. Fat saturated MRI did not show enhancement ofthe optic nerve nor any brain abnormalities or mass lesions. He had a normal lab workup includingCBC, BMP, quantiferon gold, B12, RPR, and ACE and a normal CXR. On follow up one month later,he experienced no vision improvement. At this point, testing for Lebers hereditary optic neuropathy(LHON) was performed and was negative. He returned 6 months later with subjective worsening ofvision in the right eye, however acuity was stable at 4/200. He was started on IVIg therapy andautoimmune and NMO antibodies were drawn. Antibody testing was negative and on follow up onemonth later, his acuity remained unchanged and his scotoma was larger and denser. He was again lost tofollow up for 3 years until he began losing vision in the left eye. Exam revealed counting fingers visionin the right eye and 20/40 with a temporal visual field defect in the left eye. MRI showed an enhancingmass extending from the planum tuberculum and suprasellar area to the right temporal lobe and intoboth orbits. A procedure was performed

A 44-Year-Old Man With Bilateral Optic Neuropathy, Optic Nerve Sheath Enhancement, and Cardiac Dysfunction

In this issue of the Journal of Neuro-Ophthalmology, M. Tariq Bhatti, MD and Mark Moster, MD discuss the following 6 articles

Neurosarcoidosis masquerading as meningioma

Sarcoidosis is a multisystem inflammatory disease that can affect the central and/or peripheral nervous system approximately 5-15% of the time. When the nervous system is involved, there are a variety of ophthalmic manifestations that can be seen including cranial nerve palsies, direct optic nerve involvement or papilledema. Here we present a case of a diagnostically challenging case of neurosarcoidosis