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

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

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

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

Retrograde Degeneration of Retinal Ganglion Cells in Homonymous Hemianopia

"To demonstrate the relationship between topographic reduction in macular ganglion cell complex (GCC) thickness as detected with spectral-domain optical coherence tomography (SD-OCT) to visual field defects caused by ischemic occipital cortical injury.

Where the Lung Meets the Eye

"The cavernous sinus is an important neurovascular crossing point. Careful examination of patients presenting with multiple cranial neuropathies may suggest a lesion of this region but the differential is wide and often difficult to confirm.1 Potential infectious and inflammatory etiologies as well as local malignant invasion should be addressed. However, metastases from distant sites are more rarely seen.

Cigarette Smoking and Activities of Daily Living in Ocular Myasthenia Gravis

"Myasthenia Gravis (MG) is an autoimmune disorder of the neuromuscular junction most often caused by autoantibodies targeting the acetylcholine receptor (AChR). Cigarette smoking is known to affect neuronal AChRs and it has been shown to influence other autoimmune diseases, but the effect of cigarette smoking on MG has not been thoroughly investigated.