|Year : 2018 | Volume
| Issue : 2 | Page : 94-102
Optical coherence tomography in neurophthalmology
JK Ann, Ani Sreedhar, Rita Mary Tomy, Dona Ann Mathew
Little Flower Hospital and Research Centre, Angamaly, Kerala, India
|Date of Web Publication||28-Aug-2018|
J K Ann
ACN 19, Anchorage, Opposite Santhi Bhavan Orphanage, Angamaly, Ernakulam - 683 572, Kerala
Source of Support: None, Conflict of Interest: None
Optical coherence tomography (OCT), widely used in the management of macular disorders and glaucoma, has proved its usefulness in many neurophthalmic disorders. OCT can quantify the retinal nerve fiber layer thickness and ganglion cell layer thickness and provides an idea about the neuronal integrity of the anterior visual pathway, which cannot be picked up by routine fundoscopy. Here, we are discussing some neurophthalmic and neurologic diseases where OCT can contribute to the diagnosis, disease monitoring and can provide prognostic information.
Keywords: Ganglion cell layer, neurophthalmology, optical coherence tomography, retinal nerve fiber layer
|How to cite this article:|
Ann J K, Sreedhar A, Tomy RM, Mathew DA. Optical coherence tomography in neurophthalmology. Kerala J Ophthalmol 2018;30:94-102
| Introduction|| |
Optical coherence tomography (OCT) is a noninvasive, noncontact technique that uses low-coherence interferometry to obtain high-resolution cross-sectional images of the anterior and posterior segments of the eye. Widely used in the management of glaucoma and retinal disorders, OCT is now gaining popularity in the diagnosis and monitoring of several neuro-ophthalmological and neurological conditions.
| Principles of Optical Coherence Tomography|| |
“Interference” is a phenomenon that occurs when electromagnetic waves are superimposed on each other and interferometry uses this physical property to measure optical delay on a micron scale. Infrared rays (wavelength 820 nm) generated by a superluminescent diode are split into two arms by a coupler. The one arm, called the reference arm, the rays are reflected by a mirror back along its original path, whereas in the other arm, called the sample arm, the rays are reflected back through the eye being imaged. The rays are scattered to varying extents by the layers of the eye which have different refractive indices. The returning rays are recombined with the sample beam to produce an interference pattern that can be recorded and analyzed by a decoder to generate images. A spatial resolution of 1–15 μm can be obtained by OCT, far sharper than the resolution of 300 μm to 1 mm obtained by high-resolution computed tomography or magnetic resonance imaging (MRI) scans. The first commercially available OCT systems were time-domain (TD-OCT), but this has been superseded by spectral domain OCT (SD-OCT) where images are captured at greater speed with better definition and reduced movement artifacts. SD-OCT (also known as Fourier domain OCT) is a spectrometer-based technique that uses Fourier transformation to convert the obtained signals into images. The OCT machine has built-in algorithms to measure retinal thickness, peripapillary retinal nerve fiber layer (RNFL) thickness and ganglion cell layer (GCL) thickness and to quantify optic nerve head morphology. To the neuroophthalmologist, the most useful OCT parameters are the peripapillary RNFL thickness and the GCL thickness.
| Factors Affecting Scan Accuracy|| |
OCT images may be affected by results of poor fixation, poor centration, and movement artifacts. Other factors affecting scan accuracy include as follows:.
An OCT measurement is only reliable if the signal strength is good. A signal strength of 7/10 is generally considered acceptable. Signal strength may be reduced by media opacity due to corneal scars, cataract or vitreous opacities, and by contact lenses.
Obtaining a good image is easier in a dilated pupil, but pupillary diameter does not significantly affect OCT measurements unless < 3 mm.
Compared to emmetropic patients, RNFL is thinner in high myopes and may have a different distribution.
| Uses of Optical Coherence Tomography in Neuro-Ophthalmological Practice|| |
In neuro-ophthalmology, OCT can aid in diagnosis, monitoring and in some cases, provide prognostic information concerning diseases affecting the optic nerve. In addition, OCT is emerging as an important tool in diagnosis and monitoring of neurodegenerative conditions such as Alzheimer's dementia and Parkinson's disease. Ganglion cells are concentrated in the macula and loss of macular volume and thinning of the ganglion layer, detectable by OCT, suggests damage to these first-order neurons in the visual afferent pathway. Unmyelinated axons of the retinal ganglion cells make up the RNFL and reduction in the RNFL thickness can, therefore, be inferred to be due to axonal damage.
| Optic Disc Swelling|| |
OCT provides reliable and quantitative information about optic disc edema and structural changes during the resolution of optic nerve head swelling. It can help to differentiate visual loss associated with disc edema due to optic neuropathy from that due to maculopathy and guide management decisions. A more aggressive approach is mandated if visual loss is due to optic neuropathy than in more benign, reversible macular abnormalities such as subfoveal fluid or choroidal folds.
| Papilledema|| |
Papilledema refers to swelling of the optic disc in the context of elevated intracranial pressure. The utility of OCT in the diagnosis and grading of papilledema has been revealed by Scott et al. These patients usually have neurological symptoms, deficits and imaging abnormalities related to their underlying condition. An ophthalmologist often encounters papilledema secondary to idiopathic intracranial hypertension where isolated visual abnormalities without neurological deficits occur in over 80% of patients. In optic disc swelling secondary to idiopathic intracranial hypertension, perimetric sensitivity losses tend to be greater in eyes with more edema. Visual loss in IIH may be permanent if not detected and treated in time. OCT may be useful in detecting early papilledema, monitoring the course of the illness and studying the effects of therapy. In the acute stage, marked elevations in RNFL thickness and macular volumes are seen. As the edema resolves RNFL values decline and as the condition becomes more chronic, there is a decrease in GCL and RNFL values as well as macular volumes.
| Pseudopapilledema|| |
A false appearance of papilledema referred to as “pseudopapilledema” may be seen in optic nerve head drusen (ONHD) and other conditions. Differentiating optic disc edema caused by papilledema or other optic neuropathies from pseudopapilledema by ophthalmoscopy is challenging. Fluorescein angiography, B-scan ultrasonography, and computed tomography are often used in this setting, but OCT may play an important ancillary role.
Pseudopapilledema due to optic nerve head drusen
Both RNFL and macular ganglion cell and inner plexiform layer (GCIPL) analysis reveal significant thinning in eyes with ONHD. As drusen develop and become superficial, the RNFL thickness decreases. A direct correlation is noted between OCT measurements, numbers of clinically visible ONHD and visual field defects. Savini et al. identified a hyporeflective space located between the sensory retina and the retinal pigment epithelium and choriocapillaris complex (subretinal hypo-reflective space [SHYPS]) in patients with optic disc edema. They noted that the SHYPS differs in OCT images of ONHD. In true disc edema, the optic nerve head generally had a smooth internal contour and the SHYPS was thickest near the optic nerve head followed by a gradual tapering away from the optic nerve to form a recumbent “lazy V” pattern. However, the optic nerve head in ONHD generally had a “lumpy-bumpy” internal contour with an abrupt decline in the SHYPS.
| Optic Neuropathies|| |
Optic neuropathies may be due to compressive, toxic, nutritional, ischemic, infiltrative, infective, or other inflammatory causes. Inflammatory optic neuritis may occur as an isolated sporadic event or in the context of diseases such as multiple sclerosis (MS), neuromyelitis optica (NMO), or acute disseminated encephalomyelitis.
OCT confirms the presence of optic disc edema in anterior ON and quantifies the severity of axonal loss that follows the acute episode regardless of etiology.
Most patients with sporadic or isolated optic neuritis or ON due to MS recover normal visual function although subtle defects in motion perception and low contrast spatial discrimination persist. The use of OCT in assessing structural injury to the optic nerve in the acute stage of ON and the prognosticating outcome has been explored. In the acute stage, impaired axoplasmic flow causes peripapillary edema and elevated RNFL thickness. This masks any thinning that may result from axonal loss. The RFNL thickness declines in the months after ON as the swelling subsides. Functional visual outcomes at 6–12 months after acute ON correlate well with OCT parameters such as RNFL and GCL thickness and macular volume, but their predictive value in the acute stage is unsatisfactory. Another limitation of OCT is that RNFL measures do not usually decrease below 30 μm regardless of the severity of the injury and hence may not be useful as markers of further progression of optic nerve damage or recurrence of optic neuritis [Figure 1].
|Figure 1: (a) Humphrey field analyzer (30-2) of a patient with BE optic neuritis after 1 month left eye showing peripheral constriction of visual field, right eye showing supero nasal peripheral field defect. (b) Cirrus optical coherence tomography centered around optic disc retinal nerve fiber layer - corresponding thinning (depicted in red) in retinal nerve fiber layer in both eyes, left eye shows more severe thinning which correlates with the field loss. (c) Ganglion cell analysis showing both eyes ganglion cell layer thinning, more in left eye|
Click here to view
Optic neuritis may be the harbinger or first clinical manifestation of MS in 20% of patients, and a sensitive tool to differentiate sporadic, isolated ON from a clinically isolated syndrome presaging MS is of paramount significance. OCT which can detect subclinical axonal loss in eyes with normal visual fields and normal visual acuity  has been found to be useful in this context. RNFL loss has been demonstrated even in the asymptomatic eye of MS patients with unilateral ON, although less than in the affected eye. Petzold et al. reported, on meta-analysis of TD-OCT data, that RNFL thickness was reduced on an average by 7.08 μm in the unaffected eye of MS patient as against 20.38 μm in the eye affected by ON and that it was more pronounced in the temporal quadrant. Studies using newer SD-OCT techniques also corroborate previous findings that RNFL thinning generally occurs in the temporal quadrant.
The optic neuritis treatment trial showed a higher incidence of retrobulbar neuritis in patients with MS.
In retrobulbar neuritis, where the optic disc appears normal clinically, OCT shows changes in peripapillary RNFL and may improve diagnostic certainty.
Although it has been suggested that OCT may be useful in differentiating between the remitting-relapsing and primary progressive sub-types of MS, its application in this setting has to be explored further. Regardless of sub-type, RNFL thickness correlates with visual function such as visual acuity at both low- and high-contrast, visual field, and color vision.
OCT is increasingly used to study disease progression even in the absence of clinical or radiologically evident relapses. Narayanan et al. reported RNFL decline of 1.49 μm/years in unaffected eyes of patients with MS. Interestingly, OCT findings also correlated with brain atrophy and neurological disability in these patients suggesting that OCT may be used to monitor neurodegeneration.
Microcystic macular edema (MME) and thickening of the inner nuclear layer on OCT is associated with disease activity and worse disability in MS and can predict disease progression in patients with MS. However, this finding is not specific for demyelinating disease; it can be found in numerous disorders such as compressive, nutritional/toxic, and hereditary optic neuropathies.
SD-OCT is also a useful tool for the diagnosis of macular edema that could appear in MS patients taking Fingolimod or in those affected by intermediate uveitis.
In addition to monitoring axonal damage, OCT may predict visual recovery in MS patients, Costello et al. found a threshold of RNFL thickness (75 μm) with TD-OCT below which RNFL measurements predicted persistent visual dysfunction.
OCT has been included in the most recent MS clinical trials, and now is considered essential for noninvasively assessing the effectiveness of therapies that reduce axonal and neuronal loss by neuroprotective or myelin repair mechanisms.
Axonal loss in the optic nerve is greater and visual prognosis poorer after an episode of ON in patients with NMO, an autoimmune condition characterized by the presence of antibodies directed against aquaporin-4 water channel proteins on the cell membrane. Findings on OCT, although not conclusive in differentiating between MS and NMO, nevertheless reveal interesting differences between the two conditions. The RNFL thickness, macular volume, and GCL thickness are lower in NMO compared to MS. Patients with NMO have a reduction of 55–83 μm in RNFL values as against a loss of 20 μm typically seen in MS. Unlike MS associated optic neuritis which preferentially affects the temporal fields, it has also been shown that the superior and inferior quadrants are more intensely affected after NMO. Furthermore unlike MS, unaffected eyes in patients with NMO do not have RNFL thinning. MME on OCT is also encountered far more commonly in NMO than in MS or sporadic ON.
Anterior ischemic optic neuropathy
Anterior ischemic optic neuropathy (AION) is characterized by sudden visual loss resulting from hypo-perfusion or nonperfusion of posterior ciliary arteries. OCT may prove an objective tool to assess new therapies arising in the future for this devastating disorder. At the onset, a relative afferent pupillary defect and disc swelling can be seen on fundoscopy. Over the first 3 months, the optic nerve head swelling resolves until degeneration of axons and apoptosis of ganglion cell bodies in the retina results in optic nerve head atrophy. SD-OCT allows in vivo measurements and monitoring of peripapillary RNFL thickness and macular thickness in various stages of the disease process. Studies have shown a moderate-to-strong correlation between peripapillary RNFL loss and corresponding visual field loss.,,,, Correlations also exist between the visual field and whole macular thickness measured 6 months after the acute event., RNFL measurements obtained closer to the acute episode may underestimate the amount of true damage due to the edema and resultant swelling that could mask the true degree of RNFL thinning. The macular thickness and GCL changes are not influenced by the optic nerve edema and could be more useful for detecting the structural changes in the 1st month than RNFL evaluation. Kupersmith revealed that only 10% of eyes with non-AION (NAION) had RNFL loss, whereas 76% had GCIPL thinning at 1 month. Therefore, GCL thinning can be detected before RNFL loss and could be a biomarker of early structural loss in AION. Macular analysis by OCT can reveal subretinal fluid in around 12% of patients with NAION. This may contribute to some of the visual loss associated with NAION and could account for some of the visual improvement that can follow after its resolution  [Figure 2].
|Figure 2: (a) Fundus photo after acute episode of anterior ischemic optic neuropathy right eye. (b) Humphrey field analyzer (30-2) showing superior altitudinal scotoma right eye. (c) Cirrus optical coherence tomography centered around optic disc with peripapillary retinal nerve fiber layer showing normal thickness both eyes (depicted in white and green). (d) But ganglion cell layer thickness is less in the right eye – inferior and infero temporal areas (depicted in yellow and green) which correspond to the superior field defect in right eye. Retinal nerve fiber layer fails to show the thinning because it is being masked by edema|
Click here to view
| Optic Neuropathy Due to Other Causes|| |
In traumatic optic neuropathy, OCT can reveal RNFL loss from 2 to 4 weeks after trauma and may be useful for monitoring and prognostication.
In toxic and nutritional optic neuropathies, RNFL thickness may be normal or slightly increased on initial evaluation and become thinned, especially temporally, on subsequent testing  [Figure 3].
|Figure 3: (a) Visual field of a toxic optic neuropathy showing enlargement of blind spot in left eye and a papillo macular bundle defect in right eye. (b) Retinal nerve fiber layer shows severe loss of thickness in temporal and also in superior, and inferior quadrants. (c) Ganglion cell layer of both eye shows severe thinning in all quadrants|
Click here to view
The observed thinning of the temporal RNFL corresponds to the more significant involvement of the papillo-macular fibers.
| Pituitary Tumours|| |
Space-occupying lesions of the brain may cause visual dysfunction due to compression of the visual pathways, especially in the vicinity of the chiasm. The most common among these are pituitary tumors which typically cause bitemporal hemianopia and progressive visual loss [Figure 4]. OCT may help in detection of presymptomatic pituitary tumors as well as aid in their management.
|Figure 4: (a) fundus photograph of a patient with pituitary tumor causing bilateral optic atrophy. (b) Optical coherence tomography showing retinal nerve fiber layer atrophy. (c) Optical coherence tomography showing ganglion cell layer atrophy. (d) Left eye temporal visual field loss. Right eye vision is very poor to record visual field|
Click here to view
Impaired GCL thickness in the nasal half of the retina in patients undergoing OCT as part of the routine ophthalmic evaluation or glaucoma assessment raises suspicion of chiasmal compression by a pituitary tumor  and warrants imaging. Surgical intervention in otherwise asymptomatic nonsecretory pituitary tumors may be dictated by evidence of visual dysfunction. OCT abnormalities in these patients are evident before symptomatic visual loss or abnormalities on perimetry and monitoring of vision with interval OCTs may be more cost-effective than serial MRIs and more relevant to planning surgical intervention.
OCT has a potential role in detecting RNFL loss and can be used as a tool for determining visual prognosis in the case of pituitary adenoma. Studies have shown that patients with normal RNFL thickness have greater potential for visual field improvement after adenoma removal, whereas RNFL thinning (<5th percentile) predicts incomplete recovery after treatment.
| Alzheimer's Disease|| |
Alzheimer's disease (AD) is the most common cause of dementia worldwide, and its incidence is increasing. AD may be preceded by a period of minimal cognitive impairment (MCI) where mild memory disturbances are present, but the patient can independently carry out activities of daily living and function normally socially. Not all patients with MCI go on to develop AD. Clinical and histological studies of AD patients suggest that the neurodegenerative process in the brain also affects the retina early. A significant reduction of RNFL thickness has been reported in patients with AD compared with healthy controls. It has been suggested that the plaques may be detected in the retina early in the disease before the onset of clinical dementia and examination with fundus auto-fluorescence and OCT may be a valuable supplement to neurological testing in patients with minimal cognitive impairment (MCI) and may help predict progression to dementia.
| Parkinson's Disease|| |
Parkinson's disease (PD) is a neurodegenerative condition characterized by selective loss of dopaminergic neurons, mainly in the basal ganglia. RNFL and macular thickness are significantly reduced in patients with PD and correlate with PD severity., SD-OCT is a valid and reproducible device for detecting subclinical RNFL atrophy in these patients. Newer segmentation algorithm of the Spectralis OCT revealed retinal layer atrophy especially in the inner layers of patients with longer disease duration. Spund et al. in their study have reported that the foveal pit is thinner and broader in PD and have suggested that this remodeling of the foveal architecture may represent a visible and quantifiable signature of the disease.
| Newer Modalities|| |
Newer OCT such as Doppler OCT and OCT angiography (OCTA) are useful tools for vascular evaluation of eye diseases, including optic neuropathies.
Doppler OCT measures the Doppler shift of the reflected light. It has been used to measure total retinal blood flow. In glaucomatous and nonglaucomatous optic neuropathies, Doppler OCT has showed decreased retinal blood flow rate and velocity., OCTA can image slow transverse flow in capillaries by detecting the variation or decorrelation of OCT signal between cross-sectional images. It uses the intrinsic contrast of moving blood cells, and no dye injection is needed. OCTA has been used to investigate several neurodegenerative and nonglaucomatous optic nerve diseases with vascular components. In MS, OCTA of the optic disc has shown reduced flow index and vessel density in eyes with optic neuritis compared with normal subjects, as well as MS eyes without a history of optic neuritis. However, mean parafoveal flow index did not differ significantly among different groups.
OCTA can noninvasively visualize microvascular flow impairment in patients with NAION. Flow impairment was seen on OCTA in the retinal peripapillary capillaries and peripapillary choriocapillaries corresponded to structural OCT deficits of the RNFL and GCL complex and to automated visual field deficits in most of the eyes.
| Conclusion|| |
The indications and uses of OCT in neuro-ophthalmological diagnosis, prognostication, and monitoring of progression or treatment effect are continuing to expand, and it is recognized as a vital tool in the armamentarium of the neuro-ophthalmologist.
The author would like to thank Dr. Ashok Menon, Consultant neurologist, Little Flower hospital Angamaly.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Scott CJ, Kardon RH, Lee AG, Frisén L, Wall M. Diagnosis and grading of papilledema in patients with raised intracranial pressure using optical coherence tomography vs. clinical expert assessment using a clinical staging scale. Arch Ophthalmol 2010;128:705-11.
Rebolleda G, Muñoz-Negrete FJ. Follow-up of mild papilledema in idiopathic intracranial hypertension with optical coherence tomography. Invest Ophthalmol Vis Sci 2009;50:5197-200.
Savini G, Bellusci C, Carbonelli M, Zanini M, Carelli V, Sadun AA, et al.
Detection and quantification of retinal nerve fiber layer thickness in optic disc edema using stratus OCT. Arch Ophthalmol 2006;124:1111-7.
Johnson LN, Diehl ML, Hamm CW, Sommerville DN, Petroski GF. Differentiating optic disc edema from optic nerve head drusen on optical coherence tomography. Arch Ophthalmol 2009;127:45-9.
Noval S, Contreras I, Rebolleda G, Muñoz-Negrete FJ. Optical coherence tomography versus automated perimetry for follow-up of optic neuritis. Acta Ophthalmol Scand 2006;84:790-4.
Petzold A, de Boer JF, Schippling S, Vermersch P, Kardon R, Green A, et al.
Optical coherence tomography in multiple sclerosis: A systematic review and meta-analysis. Lancet Neurol 2010;9:921-32.
Rebolleda G, Diez-Alvarez L, Casado A, Sánchez-Sánchez C, de Dompablo E, González-López JJ, et al.
OCT: New perspectives in neuro-ophthalmology. Saudi J Ophthalmol 2015;29:9-25.
Narayanan D, Cheng H, Bonem KN, Saenz R, Tang RA, Frishman LJ, et al.
Tracking changes over time in retinal nerve fiber layer and ganglion cell-inner plexiform layer thickness in multiple sclerosis. Mult Scler 2014;20:1331-41.
Saidha S, Sotirchos ES, Ibrahim MA, Crainiceanu CM, Gelfand JM, Sepah YJ, et al.
Microcystic macular oedema, thickness of the inner nuclear layer of the retina, and disease characteristics in multiple sclerosis: A retrospective study. Lancet Neurol 2012;11:963-72.
Costello F, Hodge W, Pan YI, Eggenberger E, Coupland S, Kardon RH, et al.
Tracking retinal nerve fiber layer loss after optic neuritis: A prospective study using optical coherence tomography. Mult Scler 2008;14:893-905.
Bennett JL, de Seze J, Lana-Peixoto M, Palace J, Waldman A, Schippling S, et al.
Neuromyelitis optica and multiple sclerosis: Seeing differences through optical coherence tomography. Mult Scler 2015;21:678-88.
Monteiro ML, Fernandes DB, Apóstolos-Pereira SL, Callegaro D. Quantification of retinal neural loss in patients with neuromyelitis optica and multiple sclerosis with or without optic neuritis using fourier-domain optical coherence tomography. Invest Ophthalmol Vis Sci 2012;53:3959-66.
Hattenhauer MG, Leavitt JA, Hodge DO, Grill R, Gray DT. Incidence of nonarteritic anterior ischemic optic neuropathy. Am J Ophthalmol 1997;123:103-7.
Contreras I, Noval S, Rebolleda G, Muñoz-Negrete FJ. Follow-up of nonarteritic anterior ischemic optic neuropathy with optical coherence tomography. Ophthalmology 2007;114:2338-44.
Contreras I, Rebolleda G, Noval S, Muñoz-Negrete FJ. Optic disc evaluation by optical coherence tomography in nonarteritic anterior ischemic optic neuropathy. Invest Ophthalmol Vis Sci 2007;48:4087-92.
Deleón-Ortega J, Carroll KE, Arthur SN, Girkin CA. Correlations between retinal nerve fiber layer and visual field in eyes with nonarteritic anterior ischemic optic neuropathy. Am J Ophthalmol 2007;143:288-94.
Hood DC, Anderson S, Rouleau J, Wenick AS, Grover LK, Behrens MM, et al.
Retinal nerve fiber structure versus visual field function in patients with ischemic optic neuropathy. A test of a linear model. Ophthalmology 2008;115:904-10.
Bellusci C, Savini G, Carbonelli M, Carelli V, Sadun AA, Barboni P, et al.
Retinal nerve fiber layer thickness in nonarteritic anterior ischemic optic neuropathy: OCT characterization of the acute and resolving phases. Graefes Arch Clin Exp Ophthalmol 2008;246:641-7.
Fernández-Buenaga R, Rebolleda G, Muñoz-Negrete FJ, Contreras I, Casas-Llera P. Macular thickness. Ophthalmology 2009;116:1587, 1587.e1-3.
Papchenko T, Grainger BT, Savino PJ, Gamble GD, Danesh-Meyer HV. Macular thickness predictive of visual field sensitivity in ischaemic optic neuropathy. Acta Ophthalmol 2012;90:e463-9.
Rebolleda G, de Dompablo E, Muñoz-Negrete FJ. Ganglion cell layer analysis unmasks axonal loss in anterior optic neuritis. J Neuroophthalmol 2015;35:165-7.
Hedges TR 3rd
, Vuong LN, Gonzalez-Garcia AO, Mendoza -Santiesteban CE, Amaro-Quierza ML. Subretinal fluid from anterior ischemic optic neuropathy demonstrated by optical coherence tomography. Arch Ophthalmol 2008;126:812-5.
Yum HR, Park SH, Park HY, Shin SY. Macular ganglion cell analysis determined by cirrus HD optical coherence tomography for early detecting chiasmal compression. PLoS One 2016;11:e0153064.
Danesh Meyer H, Wong A, Matheos K, Stylli S, Nicholas A, Frampton C, et al
. Optical coherence tomography predicts visual outcome for pituitary tumors. Journal of Clinical Neuroscience 2015;22:1098-1104.
Sergott RC, Kayabasi U. Progression of plaques in retina with dementia in Alzheimerŕs disease. In: 40th
NANOS (North American Neuro-Ophthalmology Society) Meeting. Rio Grande, Puerto Rico, USA: Annual Meeting Syllabus; 2014. p. 148.
Satue M, Seral M, Otin S, Alarcia R, Herrero R, Bambo MP, et al.
Retinal thinning and correlation with functional disability in patients with Parkinson's disease. Br J Ophthalmol 2014;98:350-5.
Garcia-Martin E, Larrosa JM, Polo V, Satue M, Marques ML, Alarcia R, et al.
Distribution of retinal layer atrophy in patients with Parkinson disease and association with disease severity and duration. Am J Ophthalmol 2014;157:470-8.
Spund B, Ding Y, Liu T, Selesnick I, Glazman S, Shrier EM, et al.
Remodeling of the fovea in Parkinson disease. J Neural Transm (Vienna) 2013;120:745-53.
Wang Y, Fawzi AA, Varma R, Sadun AA, Zhang X, Tan O, et al.
Pilot study of optical coherence tomography measurement of retinal blood flow in retinal and optic nerve diseases. Invest Ophthalmol Vis Sci 2011;52:840-5.
Jia Y, Wei E, Wang X, Zhang X, Morrison JC, Parikh M, et al.
Optical coherence tomography angiography of optic disc perfusion in glaucoma. Ophthalmology 2014;121:1322-32.
Wang X, Jia Y, Spain R, Potsaid B, Liu JJ, Baumann B, et al.
Optical coherence tomography angiography of optic nerve head and parafovea in multiple sclerosis. Br J Ophthalmol 2014;98:1368-73.
Wright Mayes E, Cole ED, Dang S, Novais EA, Vuong L, Mendoza-Santiesteban C, et al.
Optical coherence tomography angiography in nonarteritic anterior ischemic optic neuropathy. J Neuroophthalmol 2017;37:358-64.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]