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Jeffrey M Gelfand - One of the best experts on this subject based on the ideXlab platform.
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reply microcysts in the Inner Nuclear Layer from optic atrophy are caused by retrograde trans synaptic degeneration combined with vitreous traction on the retinal surface
Brain, 2013Co-Authors: Ari J Green, Daniel M Schwartz, Jeffrey M GelfandAbstract:ARTICLE Sir, We appreciate the thoughtful commentary from Drs Lujan and Horton (2013) based on their patient with Kjer’s dominant optic atrophy with retinal Inner Nuclear Layer microcysts. Their case highlights an emerging understanding that Inner Nuclear microcysts are not specific to multiple sclerosis. We—and others—have now identified them in neuromyelitis optica (Gelfand et al. , 2013; Sotirchos et al. , 2013) and they have been reported to occur in neurofibromatosis 1-associated optic nerve glioma (Abegg et al. , 2012), dominant optic atrophy and Leber’s hereditary optic neuropathy (Barboni et al. , 2013). Anecdotally, we have also heard of individual cases in patients with nerve atrophy following papilledema and traumatic optic neuropathy. However—other than for neuromyelitis optica—the frequency with which the microcysts occur in non-multiple sclerosis optic neuropathy remains unclear, and we are not aware of any cases of retinal Inner Nuclear Layer microcysts that have been described in the most common optic neuropathy, glaucoma. Lujan and Horton (2013) assert that these Inner Nuclear Layer microcystic changes are related to trans-synaptic cell loss based on pathological reports that highlight Inner Nuclear Layer cell loss in multiple sclerosis (Gills and Wadsworth, 1967; Green et al. , 2010) and after other forms of optic nerve injury (Van …
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microcystic Inner Nuclear Layer abnormalities and neuromyelitis optica
JAMA Neurology, 2013Co-Authors: Jeffrey M Gelfand, Bruce Ac Cree, Rachel Nolan, Sam Arnow, Ari J GreenAbstract:Importance Microcystic abnormalities involving the Inner Nuclear Layer of the retina occurs in a subset of patients with multiple sclerosis, most commonly in eyes previously affected by symptomatic optic neuritis. Acute optic neuritis is a cardinal manifestation of neuromyelitis optica (NMO). To our knowledge, microcystic Inner Nuclear Layer abnormalities have not been investigated in NMO. Objective To establish whether microcystic Inner Nuclear Layer abnormalities occur in NMO. Design Observational, retrospective study. Setting University of California at San Francisco Multiple Sclerosis Center (academic specialty clinic). Patients Twenty-five consecutive patients with NMO based on 2006 diagnostic criteria or with NMO spectrum disease (defined by seropositivity for anti–aquaporin 4 IgG in the context of a single episode of transverse myelitis or optic neuritis). Exposure Spectral-domain optical coherence tomography. Main Outcomes and Measures Identification of microcystic Inner Nuclear Layer pathology on spectral-domain optical coherence tomography. Multivariable linear regression was used to examine associations between microcystic changes and measures of retinal structure and function. The hypothesis was generated prior to the data being reviewed and analyzed. Results Microcystic changes were identified in 5 of 25 patients with NMO (20%) and 7 of 48 total eyes, including 7 of 29 eyes (24%) previously affected by optic neuritis. Microcystic changes occurred exclusively in eyes with a history of acute symptomatic optic neuritis (100% of eyes with microcystic changes had experienced prior optic neuritis compared with 71% of NMO eyes without microcystic abnormalities). There were no significant differences between patients with NMO with and without microcystic changes in terms of age, sex, and aquaporin 4–IgG antibody status. The mean age in this cohort was 44 years (range, 13-81 years); 84% were women; 80% were aquaporin 4–IgG seropositive; and the median Expanded Disability Status Scale score was 4.0 (interquartile range, 3.0-6.5). Conclusions and Relevance Microcystic Inner Nuclear Layer pathology occurs in a proportion of patients with NMO in eyes previously affected by acute optic neuritis. Additional research is needed to understand the cause of this retinal pathology and determine whether it contributes to persistent visual disability in patients with NMO following optic neuritis.
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microcystic macular oedema thickness of the Inner Nuclear Layer of the retina and disease characteristics in multiple sclerosis a retrospective study
Lancet Neurology, 2012Co-Authors: Shiv Saidha, Jeffrey M Gelfand, Elias S Sotirchos, Mohamed Ibrahim, Ciprian M Crainiceanu, Yasir J Sepah, John N Ratchford, Jiwon Oh, Michaela A Seigo, Scott D NewsomeAbstract:Summary Background Microcystic macular oedema (MMO) of the retinal Inner Nuclear Layer (INL) has been identified in patients with multiple sclerosis (MS) by use of optical coherence tomography (OCT). We aimed to determine whether MMO of the INL, and increased thickness of the INL are associated with disease activity or disability progression. Methods This retrospective study was done at the Johns Hopkins Hospital (Baltimore, MD, USA), between September, 2008, and March, 2012. Patients with MS and healthy controls underwent serial OCT scans and clinical assessments including visual function. OCT scanning, including automated intraretinal Layer segmentation, yielded thicknesses of the retinal nerve fibre Layer, the ganglion cell Layer plus Inner plexiform Layer, the INL plus outer plexiform Layer (the combined thickness of these Layers was used as a surrogate measure of INL thickness), and the outer Nuclear Layer. Patients with MS also underwent annual brain MRI scans. Disability scores were compared with the Wilcoxon rank-sum test. Mixed-effects linear regression was used to compare OCT measures and letter-acuity scores. Logistic regression was used to examine the relations of baseline OCT thicknesses with clinical and radiological parameters. Findings 164 patients with MS and 60 healthy controls were assessed. Mean follow-up was 25·8 months (SD 9·1) for patients with MS and 22·4 months (11·4) for healthy controls. Ten (6%) patients with MS had MMO during at least one study visit; MMO was visible at baseline in four of these patients. Healthy controls did not have MMO. Patients with MS and MMO had higher baseline MS severity scores (median 5·93 [range 2·44–8·91]) than those who did not have MMO at any time during the study (151 patients; 3·81 [0·13–9·47]; p=0·032), although expanded disability status scale (EDSS) scores were not significantly different (5·2 [1·0–6·5] for patients with MS and MMO vs 2·5 [0·0–8·0] for those without MMO; p=0·097). The eyes of patients with MS and MMO (12 eyes) versus those without MMO (302 eyes) had lower letter-acuity scores (100% contrast, p=0·017; 2·5% contrast, p=0·031; 1·25% contrast, p=0·014), and increased INL thicknesses (p=0·003) at baseline. Increased baseline INL thickness in patients with MS was associated with the development of contrast-enhancing lesions (p=0·007), new T2 lesions (p=0·015), EDSS progression (p=0·034), and relapses in patients with relapsing-remitting MS (p=0·008) during the study. MMO was not associated with disease activity during follow-up. Interpretation Increased INL thickness on OCT is associated with disease activity in MS. If this finding is confirmed, INL thickness could be a useful predictor of disease progression in patients with MS. Funding National Multiple Sclerosis Society, National Eye Institute, Braxton Debbie Angela Dillon and Skip Donor Advisor Fund.
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Reply: microcystic macular degeneration from optic neuropathy and Reply: microcystic macular oedema confirmed, but not specific for multiple sclerosis
Brain, 2012Co-Authors: Jeffrey M Gelfand, Ari J GreenAbstract:Sir, we appreciate the thoughtful comments submitted in response to our recent article describing a new retinal phenotype (microcystic macular oedema) in a subset of patients with multiple sclerosis (Gelfand et al. , 2012). We thank Balk et al. and Abegg et al. for sharing similar observations of microcystic abnormalities of the Inner Nuclear Layer in patients with optic nerve injury in the absence of multiple sclerosis. Clarification of the specificity of microcystic macular oedema will contribute towards understanding its aetiology, its relationship to optic neuropathy and its significance in multiple sclerosis. As discussed in our article, we considered two separate, but not mutually exclusive, mechanisms that could contribute to the development of microcystic macular oedema in multiple sclerosis: retinal inflammation with associated blood-retinal barrier leakage and/or trans-synaptic degeneration. We appreciate the proposition by Balk et al. that distortion or loss of Mueller cells in the Inner Nuclear Layer could be an additional contributory mechanism. This warrants more detailed investigation in future studies. We agree that microcystic changes may occur strictly as a consequence of trans-synaptic degeneration; however, the individual cases highlighted by Balk et al. and Abegg et al. should be interpreted with caution. Balk et al. note an example of microcystic Inner Nuclear Layer changes …
Ari J Green - One of the best experts on this subject based on the ideXlab platform.
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reply microcysts in the Inner Nuclear Layer from optic atrophy are caused by retrograde trans synaptic degeneration combined with vitreous traction on the retinal surface
Brain, 2013Co-Authors: Ari J Green, Daniel M Schwartz, Jeffrey M GelfandAbstract:ARTICLE Sir, We appreciate the thoughtful commentary from Drs Lujan and Horton (2013) based on their patient with Kjer’s dominant optic atrophy with retinal Inner Nuclear Layer microcysts. Their case highlights an emerging understanding that Inner Nuclear microcysts are not specific to multiple sclerosis. We—and others—have now identified them in neuromyelitis optica (Gelfand et al. , 2013; Sotirchos et al. , 2013) and they have been reported to occur in neurofibromatosis 1-associated optic nerve glioma (Abegg et al. , 2012), dominant optic atrophy and Leber’s hereditary optic neuropathy (Barboni et al. , 2013). Anecdotally, we have also heard of individual cases in patients with nerve atrophy following papilledema and traumatic optic neuropathy. However—other than for neuromyelitis optica—the frequency with which the microcysts occur in non-multiple sclerosis optic neuropathy remains unclear, and we are not aware of any cases of retinal Inner Nuclear Layer microcysts that have been described in the most common optic neuropathy, glaucoma. Lujan and Horton (2013) assert that these Inner Nuclear Layer microcystic changes are related to trans-synaptic cell loss based on pathological reports that highlight Inner Nuclear Layer cell loss in multiple sclerosis (Gills and Wadsworth, 1967; Green et al. , 2010) and after other forms of optic nerve injury (Van …
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microcystic Inner Nuclear Layer abnormalities and neuromyelitis optica
JAMA Neurology, 2013Co-Authors: Jeffrey M Gelfand, Bruce Ac Cree, Rachel Nolan, Sam Arnow, Ari J GreenAbstract:Importance Microcystic abnormalities involving the Inner Nuclear Layer of the retina occurs in a subset of patients with multiple sclerosis, most commonly in eyes previously affected by symptomatic optic neuritis. Acute optic neuritis is a cardinal manifestation of neuromyelitis optica (NMO). To our knowledge, microcystic Inner Nuclear Layer abnormalities have not been investigated in NMO. Objective To establish whether microcystic Inner Nuclear Layer abnormalities occur in NMO. Design Observational, retrospective study. Setting University of California at San Francisco Multiple Sclerosis Center (academic specialty clinic). Patients Twenty-five consecutive patients with NMO based on 2006 diagnostic criteria or with NMO spectrum disease (defined by seropositivity for anti–aquaporin 4 IgG in the context of a single episode of transverse myelitis or optic neuritis). Exposure Spectral-domain optical coherence tomography. Main Outcomes and Measures Identification of microcystic Inner Nuclear Layer pathology on spectral-domain optical coherence tomography. Multivariable linear regression was used to examine associations between microcystic changes and measures of retinal structure and function. The hypothesis was generated prior to the data being reviewed and analyzed. Results Microcystic changes were identified in 5 of 25 patients with NMO (20%) and 7 of 48 total eyes, including 7 of 29 eyes (24%) previously affected by optic neuritis. Microcystic changes occurred exclusively in eyes with a history of acute symptomatic optic neuritis (100% of eyes with microcystic changes had experienced prior optic neuritis compared with 71% of NMO eyes without microcystic abnormalities). There were no significant differences between patients with NMO with and without microcystic changes in terms of age, sex, and aquaporin 4–IgG antibody status. The mean age in this cohort was 44 years (range, 13-81 years); 84% were women; 80% were aquaporin 4–IgG seropositive; and the median Expanded Disability Status Scale score was 4.0 (interquartile range, 3.0-6.5). Conclusions and Relevance Microcystic Inner Nuclear Layer pathology occurs in a proportion of patients with NMO in eyes previously affected by acute optic neuritis. Additional research is needed to understand the cause of this retinal pathology and determine whether it contributes to persistent visual disability in patients with NMO following optic neuritis.
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Reply: microcystic macular degeneration from optic neuropathy and Reply: microcystic macular oedema confirmed, but not specific for multiple sclerosis
Brain, 2012Co-Authors: Jeffrey M Gelfand, Ari J GreenAbstract:Sir, we appreciate the thoughtful comments submitted in response to our recent article describing a new retinal phenotype (microcystic macular oedema) in a subset of patients with multiple sclerosis (Gelfand et al. , 2012). We thank Balk et al. and Abegg et al. for sharing similar observations of microcystic abnormalities of the Inner Nuclear Layer in patients with optic nerve injury in the absence of multiple sclerosis. Clarification of the specificity of microcystic macular oedema will contribute towards understanding its aetiology, its relationship to optic neuropathy and its significance in multiple sclerosis. As discussed in our article, we considered two separate, but not mutually exclusive, mechanisms that could contribute to the development of microcystic macular oedema in multiple sclerosis: retinal inflammation with associated blood-retinal barrier leakage and/or trans-synaptic degeneration. We appreciate the proposition by Balk et al. that distortion or loss of Mueller cells in the Inner Nuclear Layer could be an additional contributory mechanism. This warrants more detailed investigation in future studies. We agree that microcystic changes may occur strictly as a consequence of trans-synaptic degeneration; however, the individual cases highlighted by Balk et al. and Abegg et al. should be interpreted with caution. Balk et al. note an example of microcystic Inner Nuclear Layer changes …
Eric J Sigler - One of the best experts on this subject based on the ideXlab platform.
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Inner Nuclear Layer Cystic Changes in Phakic Fellow Eyes of Patients With Acute Pseudophakic Cystoid Macular Edema
Ophthalmic Surgery and Lasers, 2019Co-Authors: Nicole A. Pannullo, Eric J SiglerAbstract:Improvements in retinal imaging have recently elucidated structural patterns in the development of macular edema, particularly involving the Inner Nuclear Layer. Here, the authors describe two cases of isolated Inner Nuclear Layer cystic changes in the phakic fellow eye of patients with pseudophakic cystoid macular edema. Both cases improved with treatment of their fellow eye and resolution of contralateral macular edema. The authors hypothesize potential pathomechanisms for this likely common but under-recognized phenomenon. [Ophthalmic Surg Lasers Imaging Retina. 2019;50:522-524.].
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microcysts in the Inner Nuclear Layer a nonspecific sd oct sign of cystoid macular edema
Investigative Ophthalmology & Visual Science, 2014Co-Authors: Eric J SiglerAbstract:Citation: Sigler EJ. Microcysts in the Inner Nuclear Layer, a non-specific SDOCT sign of cystoid macular edema. Invest Ophthalmol Vis Sci. 2014;55:3282–3284. DOI:10.1167/ iovs.14-14056 Recently, many authors have propagated the notion that a specific form of ‘‘microcystic macular edema’’ occurs in patients with optic neuritis and optic atrophy of various etiology and is due to retrograde synaptic degeneration. The finding is isolated to the Inner Nuclear Layer on spectral-domain optical coherence tomography in most cases, and is present in a parafoveal, circumferential, and central macular distribution. This perspective critically reviews the evidence and suggests that Inner Nuclear Layer cystoid changes are an early and nonspecific indicator of typical cystoid macular edema of any cause, and that the finding is likely not a distinct entity.
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delayed onset Inner Nuclear Layer cystic changes following internal limiting membrane removal for epimacular membrane
Graefes Archive for Clinical and Experimental Ophthalmology, 2013Co-Authors: Eric J Sigler, John C Randolph, Steve CharlesAbstract:Purpose To report the rare occurrence of new Inner Nuclear Layer cystic spaces occurring in eyes treated with pars plana vitrectomy (PPV) and internal limiting membrane (ILM) removal for idiopathic epimacular membrane (EMM).
Shih-jen Chen - One of the best experts on this subject based on the ideXlab platform.
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Inner Nuclear Layer microcyst configuration distribution and visual prognosis in patients with epiretinal membrane after vitrectomy and membrane peeling
Scientific Reports, 2019Co-Authors: Ming-hung Hsieh, Shih-jen Chen, Fang-yi Tsai, Yu-bai Chou, Yi-ming Huang, De-kuang HwangAbstract:Inner Nuclear Layer(INL) microcysts at central macula are a common finding in patients with epiretinal membrane (ERM) after vitrectomy and membrane peeling. Using en face mode of optical coherence tomography (OCT) angiography, patients with ERM after surgery were retrospectively reviewed to understand the configuration and distribution of microcysts as well as their impact on visual acuity. Forty-six eligible patients were enrolled and their baseline best-corrected visual acuities improved from 20/67 to 20/29 (P < 0.01) after surgery. Twenty-eight (60.9%) patients had microcysts that appeared at a median of 5 months after the surgery and persisted for mean 16 months follow-up. The microcyst appeared as spheroidal shape with length ranged from 20 to 80 μm and widths of 80 μm in average. They tend to group in cluster with a density of 245 microcysts per mm2. The frequency of microcyst distribution was 86%, 54%, 32%, 25% and 18% at the nasal, superior, inferior, temporal quadrants and central 1 mm, respectively. Linear regression analysis showed that INL microcysts at central and temporal quadrants were associated with poorer visual acuity (P = 0.02 and P = 0.01, respectively). The presence of INL microcysts in center subfield and involved wider area is a poor prognostic factor for visual outcomes.
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Inner Nuclear Layer Microcyst Configuration, Distribution, and Visual Prognosis in Patients With Epiretinal Membrane After Vitrectomy and Membrane Peeling
Scientific Reports, 2019Co-Authors: Ming-hung Hsieh, Fang-yi Tsai, Yu-bai Chou, Yi-ming Huang, De-kuang Hwang, Shih-jen ChenAbstract:Inner Nuclear Layer(INL) microcysts at central macula are a common finding in patients with epiretinal membrane (ERM) after vitrectomy and membrane peeling. Using en face mode of optical coherence tomography (OCT) angiography, patients with ERM after surgery were retrospectively reviewed to understand the configuration and distribution of microcysts as well as their impact on visual acuity. Forty-six eligible patients were enrolled and their baseline best-corrected visual acuities improved from 20/67 to 20/29 (P
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POSTOPERATIVE Inner Nuclear Layer MICROCYSTS AFFECTING LONG-TERM VISUAL OUTCOMES AFTER EPIRETINAL MEMBRANE SURGERY.
Retina-the Journal of Retinal and Vitreous Diseases, 2016Co-Authors: Shih-jen Chen, Fang-yi Tsai, Yu-chien ChungAbstract:To investigate the risk factors and long-term visual impact of microcysts in the Inner Nuclear Layer developed after epiretinal membrane (ERM) surgery. This study used a retrospective review of medical records, operative video and images of patients who had undergone idiopathic ERM surgery with more than 12 months of follow-up. This study enrolled 44 patients (44 eyes) with ERM and a mean follow-up period of 30.2 months. The visual acuity improved from a mean of 6/22.8 to 6/12 (P < 0.001). Results indicated that a final visual acuity greater than 0.5 was associated with younger age, better preoperative visual acuity, a complete postoperative Inner segment and outer segment line, and absence of Inner Nuclear Layer microcysts. The visual acuity difference between patients with and without Inner Nuclear Layer microcysts emerged in the first month and continued throughout the entire study period. Shorter duration of visual symptoms, more severe grade of ERM with paravascular abnormalities, and retinal petechiae immediately after the peeling of the ERM are risk factors of microcysts. This study suggests that Inner Nuclear Layer microcysts are induced shortly after surgery and have long-term visual effects. Factors associated with this side effect suggest that severity, acuteness, and adhesiveness of ERM may play a significant role in visual outcomes.
Friedemann Paul - One of the best experts on this subject based on the ideXlab platform.
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optic neuritis is associated with Inner Nuclear Layer thickening and microcystic macular edema independently of multiple sclerosis
PLOS ONE, 2013Co-Authors: Falko Kaufhold, Hanna Zimmermann, Elisa Schneider, Klemens Ruprecht, Friedemann Paul, Timm Oberwahrenbrock, Alexander U BrandtAbstract:Background Microcystic macular edema (MME) and Inner Nuclear Layer thickening (INL) were described in multiple sclerosis (MS) and neuromyelitis optica (NMO) patients using optical coherence tomography (OCT). The cause of these findings is currently unknown and a relation to inflammatory or degenerative processes in the optic nerve is discussed.
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retinal Inner Nuclear Layer reflects disease severity and grey matter atrophy in secondary progressive multiple sclerosis in4 2 002
Neurology, 2013Co-Authors: Caspar F Pfueller, Hanna Zimmermann, Friedemann Paul, Timm Oberwahrenbrock, Katharina Klumbies, Alina Freing, Sebastian Papazoglou, Janleo Rinnenthal, Jens Wuerfel, J DorrAbstract:OBJECTIVE: To evaluate retinal Layer composition in secondary chronic progressive multiple sclerosis (SPMS) patients in comparison to healthy controls. To elucidate the connection between retinal alterations and MRI, magnetic resonance spectroscopy (MRS) and clinical status in SPMS. BACKGROUND: Neuroinflammatory and neurodegenerative processes are associated with retinal structure changes in MS patients. So far, MRI-based measures are the gold-standard to describe CNS neurodegeneration. Recently, changes in the retinal Layer composition and its correlation with disease activity and clinical status were reported, again suggesting the ganglion cell Layer (GCL) and the Inner Nuclear Layer (INL) as sites of specific retinal alterations. So far, the association between different retinal Layer thicknesses and MRI markers for brain atrophy, MRS and clinical properties were not investigated in a cohort of SPMS patients. DESIGN/METHODS: 28 SPMS patients were prospectively recruited from on-going clinical trials at baseline visit. Retinal Layer thicknesses were determined by spectral-domain Optical Coherence Tomography and semi-automated segmentation. MRI-based measures of brain atrophy and MRS parameters were derived from MRI scans at 1.5T. Patients9 history of MS, visual acuity, MSFC and EDSS were assessed. RESULTS: Macular retinal Layer thicknesses differed significantly between SPMS patients and healthy controls. The macular retinal nerve fibre Layer and the GCL showed the expected thinning in SPMS. The GCL thinning was associated with visual function loss and grey matter atrophy, but not with white matter damage. Importantly, the thickness of the INL, while being reduced on average in SPMS patients, showed a negative association with grey matter atrophy as well as with clinical impairment. CONCLUSIONS: Our data highlight the INL as a site of disease pathology in MS. The associations of INL changes with both clinical disease severity and grey matter atrophy suggest the INL for further investigating disease pathology and use as a potential surrogate marker for disease progression in MS. Supported by: German Research Foundation (DFG Exc 257) to CP, FP and JD. Disclosure: Dr. Pfueller has nothing to disclose. Dr. Klumbies has nothing to disclose. Dr. Freing has nothing to disclose. Dr. Oberwahrenbrock has nothing to disclose. Dr. Zimmermann has nothing to disclose. Dr. Papazoglou has nothing to disclose. Dr. Rinnenthal has nothing to disclose. Dr. Wuerfel has received personal compensation for activities with Novartis. Dr. Paul has received personal compensation for activities with Teva, Sanofi Aventis, Merck Serono, Biogen Idec, Bayer, Novartis, and the Guthy Jackson Charitable Foundation. Dr. Paul has received research support from Bayer-Schering, Merck-Serono, Teva Pharma and Novartis Pharma. Dr. Dorr has nothing to disclose. Dr. Brandt has received personal compensation for activities with Meedical as co-founder and director, from Heidelberg Engineering for speaker honoraria and from Bayer, Novartis Pharma and Biogen Idec for research and travel grants. Dr. Brandt holds stock and/or stock options in Meedical, which sponsored research in which Dr.Brandt was involved as an investigator. Dr. Brandt holds stock and/or stock options in Meedical.