Publications by authors named "Lenworth N Johnson"

25 Publications

  • Page 1 of 1

The relationship between cerebral and retinal microbleeds in cerebral amyloid angiopathy (CAA): A pilot study.

J Neurol Sci 2021 04 1;423:117383. Epub 2021 Mar 1.

Department of Biomedical and Pharmaceutical Sciences, University of Rhode Island, Kingston, RI, USA; George and Anne Ryan Institute for Neuroscience, University of Rhode Island, Kingston, RI, USA; Department of Neurology, Alpert Medical School of Brown University, Providence, RI, USA; Department of Surgery (Ophthalmology), Alpert Medical School of Brown University, Providence, RI, USA.

Background: The standard in vivo diagnostic imaging technique for cerebral amyloid angiopathy (CAA) is costly and thereby of limited utility for point-of-care diagnosis and monitoring of treatment efficacy. Recent recognition that retinal changes may reflect cerebral changes in neurodegenerative disease provides an ideal opportunity for development of accessible and cost-effective biomarkers for point-of-care use in the detection and monitoring of CAA. In this pilot study, we examined structural and angiographic retinal changes in CAA patients relative to a control group, and compared retinal and cerebral pathology in a group of CAA patients.

Methods: We used spectral domain optical coherence tomography (SD-OCT) to image the retina and compared retinal microbleeds to both cerebral microbleeds and white matter hyperintensities (WMH) in CAA patients, as seen on MRI. We compared retinal angiographic changes, along with structural retinal neuronal layer changes in CAA patients and cognitively normal older adults, and examined the relationship between retinal and cerebral microbleeds and cognition in CAA patients.

Results: We found a trend level correlation between retinal and cerebral microbleeds in CAA patients. Moreover, we found a significant correlation between retinal microbleeds and episodic memory performance in CAA patients. There were no significant group differences between CAA patients and cognitively normal older adults on retinal angiographic or structural measurements.

Conclusion: Retinal microbleeds may reflect degree of cerebral microbleed burden in CAA. This picture was complicated by systolic hypertension in the CAA group, which is a confounding factor for the interpretation of these data. Our results stimulate motivation for pursuit of a more comprehensive prospective study to determine the feasibility of retinal biomarkers in CAA.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.jns.2021.117383DOI Listing
April 2021

Change in retinal structural anatomy during the preclinical stage of Alzheimer's disease.

Alzheimers Dement (Amst) 2018 7;10:196-209. Epub 2018 Feb 7.

Interdisciplinary Neuroscience Program, University of Rhode Island, Kingston, RI, USA.

Introduction: We conducted a 27-month longitudinal study of mid-life adults with preclinical Alzheimer's disease (AD), using spectral domain optical coherence tomography to compare changes in volume and thickness in all retinal neuronal layers to those of age-matched healthy control subjects.

Methods: Fifty-six older adults (mean age = 65.36 years) with multiple risk factors for AD completed spectral domain optical coherence tomography retinal imaging and cognitive testing at baseline. Twenty-seven months later, they completed the same examinations and an F-florbetapir positron emission tomography imaging study.

Results: Compared to healthy control subjects, those in the preclinical stage of AD showed a significant decrease in macular retinal nerve fiber layer (mRNFL) volume, over a 27-month follow-up interval period, as well as a decrease in outer nuclear layer and inner plexiform layer volumes and thickness in the inferior quadrant. However, only the mRNFL volume was linearly related to neocortical positron emission tomography amyloid standardized uptake value ratio after controlling for any main effects of age ( = 0.103; ρ = 0.017). Furthermore, the magnitude of mRNFL volume reduction was significantly correlated with performance on a task of participants' abilities to efficiently integrate visual and auditory speech information (McGurk effect).

Discussion: We observed a decrease in mRNFL, outer nuclear layer, and inner plexiform layer volumes, in preclinical AD relative to controls. Moreover, the largely myelinated axonal loss in the RNFL is related to increased neocortical amyloid-β accumulation after controlling for age. Volume loss in the RNFL, during the preclinical stage, is not related to performance on measures of episodic memory or problem solving. However, this retinal change does appear to be modestly related to relative decrements in performance on a measure of audiovisual integration efficiency that has been recently advanced as a possible early cognitive marker of mild cognitive impairment.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.dadm.2018.01.003DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5956814PMC
February 2018

Increased Prevalence of Optic Disc Drusen after Papilloedema from Idiopathic Intracranial Hypertension: On the Possible Formation of Optic Disc Drusen.

Neuroophthalmology 2016 Aug 1;40(4):171-180. Epub 2016 Jul 1.

Lifespan Biostatistics Core, Departments of Orthopaedics and Surgery, Alpert Medical School of Brown University/Lifespan/Rhode Island Hospital , Providence, Rhode Island, USA.

This is a 25-year observational retrospective review of 372 consecutive participants with optic disc drusen or resolved papilloedema from idiopathic intracranial hypertension. The prevalence of optic disc drusen at 19% among eyes with resolved papilloedema was approximately 10 times higher and significantly increased ( < 0.001) as compared with the occurrence in the general population. Eyes with both resolved papilloedema and optic disc drusen had similar visual acuity and visual field outcome as compared with resolved papilloedema alone. Eyes with exposed drusen had significantly worse visual acuity and visual field outcome ( < 0.001) than buried drusen. The high prevalence of optic disc drusen after papilloedema has resolved suggests a non-coincidental relationship. Optic disc drusen formation can be a sequela of papilloedema.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1080/01658107.2016.1198917DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5123006PMC
August 2016

Nonvascular retinal imaging markers of preclinical Alzheimer's disease.

Alzheimers Dement (Amst) 2016 1;4:169-178. Epub 2016 Oct 1.

Heidelberg Engineering, Inc., Franklin, MA, USA.

Introduction: In patients with Alzheimer's disease (AD) and mild cognitive impairment, structural changes in the retina (i.e., reduced thicknesses of the ganglion cell and retinal nerve fiber layers and inclusion bodies that appear to contain beta-amyloid protein [Ab]) have been previously reported. We sought to explore whether anatomic retinal changes are detectable in the preclinical stage of AD.

Methods: A cross-sectional study (as part of an ongoing longitudinal cohort study) involving 63 cognitively normal adults, all of whom have a parent with AD and subjective memory complaints. We compared neocortical amyloid aggregation (florbetapir PET imaging) to retinal spectral domain optical coherence tomography (SD-OCT) markers of possible disease burden. Retinal biomarkers, including the number and surface area of retinal inclusion bodies and the thickness of retinal neuronal layers, were compared across groups with high vs. low neocortical beta-amyloid load.

Results: The surface area of inclusion bodies increased as a function of cortical amyloid burden. Additionally, there was a trend toward a selective volume increase in the inner plexiform layer (IPL; a layer rich in cholinergic activity) of the retina in Aβ+ relative to Aβ- participants, and IPL volume was correlated with the surface area of retinal inclusion bodies.

Discussion: These initial results suggest that retinal imaging may be a potential cost-effective and noninvasive technique that can be used to identify those at-risk for AD. Layer-specific changes in the IPL and their association with surface area of inclusion bodies are discussed as a possible reflection of early inflammatory processes associated with cholinergic disruption and concurrent Ab accumulation in the neocortex.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.dadm.2016.09.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5078641PMC
October 2016

Glaucoma as a Neurodegenerative Disease: Why We Must 'Look for the Protein'.

R I Med J (2013) 2016 Jun 1;99(6):18-21. Epub 2016 Jun 1.

Professor of Surgery (Ophthalmology), Deputy Chief of Ophthalmology, Alpert Medical School of Brown University; Rhode Island Hospital, Providence, RI.

For years, clinicians and scientists interested in glaucoma have focused on the anterior segment of the eye and lowering of the intraocular pressure with respect to glaucoma causes and therapies. Yet glaucoma progresses in many individuals despite lowering the intraocular pressure. Herein, the concept of glaucoma as a neurodegenerative disease is presented. [Full article available at http://rimed.org/rimedicaljournal-2016-06.asp, free with no login].
View Article and Find Full Text PDF

Download full-text PDF

Source
June 2016

Pseudotumor cerebri: What We Have Learned from the Idiopathic Intracranial Hypertension Treatment Trial.

R I Med J (2013) 2016 May 2;99(5):22-4. Epub 2016 May 2.

Neuro-Ophthalmologist and Professor of Surgery (Ophthalmology) at the Warren Alpert Medical School of Brown University; Deputy Chief of Ophthalmology, Rhode Island Hospital, Providence, Rhode Island.

Idiopathic intracranial hypertension, also known as pseudotumor cerebri, is an unexplained increase in intracranial pressure associated with permanent severe visual loss in 25% of cases and debilitating headaches. The condition is often associated with obesity. The Idiopathic Intracranial Hypertension Treatment Trial, a large, randomized, collaborative clinical trial, evaluated the efficacy of acetazolamide with weight loss versus placebo with weight loss in participants. Herein, we describe the major components of the clinical trial and discuss its shortcomings. [Full article available at http://rimed.org/rimedicaljournal-2016-05.asp, free with no login].
View Article and Find Full Text PDF

Download full-text PDF

Source
May 2016

Levodopa as a possible treatment of visual loss in nonarteritic anterior ischemic optic neuropathy.

Graefes Arch Clin Exp Ophthalmol 2016 Apr 20;254(4):757-64. Epub 2015 Oct 20.

Neuro-Ophthalmology Unit, Biostatistics Unit, University of Missouri-Columbia, Columbia, MO, USA.

Purpose: To determine the clinical effectiveness and potential neuroprotection of levodopa in improving visual acuity, visual field, and retinal nerve fiber layer (RNFL) thickness in eyes affected by NAION.

Method: Retrospective cohort study involving 59 eyes of 59 participants with NAION who were evaluated within 15 days of NAION onset. Participants received 25 mg carbidopa/100 mg levodopa three times daily with meals for 12 weeks (levodopa group) or were untreated (control group). Best-corrected visual acuity converted to logMAR, mean deviation (MD) threshold sensitivity on automated perimetry, and mean RNFL thickness on optical coherence tomography (OCT) were assessed. The primary outcome was the categorization of eyes into improved visual acuity (by 0.3 logMAR difference), worsened visual acuity (by 0.3 logMAR difference), or no change in visual acuity. The proportions in each category were compared between the levodopa and control groups.

Results: Among participants with 20/60 or worse initial visual acuity, levodopa-treated participants had significant improvement (P < 0.0001) in the mean change from initial to final logMAR visual acuity of -0.74 ± 0.56 (95 % CI, -0.98 to -0.50), while the mean change for the control group at -0.37 ± 1.09 (95 % confidence interval estimate, -1.00 to +0.26) was not significant (P = 0.23). A significant difference between groups was observed (P = 0.0086) such that 19/23 (83 %) in the levodopa group improved and none got worse, as compared with 6/14 (43 %) in the control group improving while four (29 %) worsened. The change in visual field MD and RNFL thickness on OCT showed no significant difference at P = 0.23 and P = 0.75 respectively. No levodopa-treated participant had any adverse event from the levodopa.

Conclusions: Treatment within 15 days of onset of NAION with levodopa improved central visual acuity by an average of 6 lines on Snellen acuity chart. Levodopa may promote neuroprotection of the maculopapular retinal ganglion cell fibers in NAION.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s00417-015-3191-zDOI Listing
April 2016

Short-term use of inhaled and intranasal corticosteroids is not associated with glaucoma progression on optical coherence tomography.

Eur J Ophthalmol 2012 Sep-Oct;22(5):695-700

Neuro-Ophthalmology Unit, Mason Eye Institute, Columbia, Missouri 65212, USA.

Purpose: To compare the changes in retinal nerve fiber layer (RNFL) thickness and optic nerve cup/disc ratio on optical coherence tomography (OCT) between users and nonusers of inhaled and intranasal corticosteroids (ICS).

Methods: Retrospective study of participants with glaucoma or glaucoma suspect having 2 or more OCTs during a 6-year period. The rates of change in Stratus OCT fast RNFL thickness scan and fast optic disc scan data were compared between ICS users and nonuser controls using random coefficient models.

Results: A total of 170 participants met the inclusion criteria, of whom 42 (25%) were ICS users and 128 (75%) were controls. The mean duration of follow-up was 3.2 years. There were no significant differences in the mean rates of change in superior RNFL (-0.8874 µm/y ICS users; -0.8592 µm/y controls; p=0.943), nasal RNFL (-0.0529 µm/y ICS users; -0.3577 µm/y controls; p=0.419), inferior RNFL (0.2703 µm/y ICS users; -0.1910 µm/y controls; p=0.165), and temporal RNFL (-0.3618 µm/y ICS users; -0.3612 µm/y controls; p=0.998) between ICS users and controls. There were no significant differences in the mean rates of change in horizontal cup/disc ratio (-0.0047 µm/y ICS users; 0.0002 µm/y controls; p=0.212) and vertical cup/disc ratio (0.0013 µm/y ICS users; 0.0029 µm/y; p=0.717) between ICS users and controls.

Conclusions: We found no significant difference in the rates of RNFL or optic nerve cup/disc ratio progression among individuals with glaucoma or glaucoma suspect following short-term ICS use.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.5301/ejo.5000141DOI Listing
December 2012

Amiodarone-associated optic neuropathy: a critical review.

Am J Med 2012 May 3;125(5):447-53. Epub 2012 Mar 3.

Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.

Although amiodarone is the most commonly prescribed anti-arrhythmic drug, its use is limited by serious toxicities, including optic neuropathy. Current reports of amiodarone-associated optic neuropathy identified from the Food and Drug Administration's Adverse Event Reporting System and published case reports were reviewed. A total of 296 reports were identified: 214 from the Adverse Event Reporting System, 59 from published case reports, and 23 from adverse events reports for patients enrolled in clinical trials. Mean duration of amiodarone therapy before vision loss was 9 months (range 1-84 months). Insidious onset of amiodarone-associated optic neuropathy (44%) was the most common presentation, and nearly one third were asymptomatic. Optic disk edema was present in 85% of cases. Following drug cessation, 58% had improved visual acuity, 21% were unchanged, and 21% had further decreased visual acuity. Legal blindness (<20/200) was noted in at least one eye in 20% of cases. Close ophthalmologic surveillance of patients during the tenure of amiodarone administration is warranted.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.amjmed.2011.09.020DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3322295PMC
May 2012

Early diabetes mellitus or hypertension is not significantly associated with severity of vision loss in nonarteritic anterior ischemic optic neuropathy.

Arch Ophthalmol 2011 Aug;129(8):1106-7

Neuro-Ophthalmology Unit, Mason Eye Institute, University of Missouri-Columbia, 65212, USA.

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1001/archophthalmol.2011.209DOI Listing
August 2011

Visual neuropraxia and progressive vision loss from thyroid-associated stretch optic neuropathy.

Eur J Ophthalmol 2010 Mar-Apr;20(2):429-36

Neuro-Ophthalmology Unit, Mason Eye Institute, University of Missouri-Columbia, Columbia, MO 65212, USA.

Purpose: Animal models have provided information on the tensile strength of the optic nerve, but to our knowledge no in vivo study of the tensile strength of the human optic nerve has been reported. Accordingly, we present 3 cases of stretch optic neuropathy, an often unrecognized cause of vision loss from thyroid eye disease.

Methods: Observational study of thyroid-associated stretch optic neuropathy.

Results: Three cases of stretch optic neuropathy were identified. Visual acuity was better than 20/40. Two patients had arcuate scotoma. Moderate to severe proptosis of 25 to 33 mm was present, without evidence of apical orbital compression. Two patients had retinal hemorrhages suggesting venous stasis retinopathy; the venous stasis retinopathy resolved after orbital decompression. Orbital decompression resulted in improvement of visual function. The rate of decibel sensitivity loss on automated perimetry was estimated at -0.042 dB/da in one case, with complete blindness projected to occur within 785 days from the onset of visual symptoms.

Conclusions: Stretch optic neuropathy presents initially as neuropraxia with temporary visual loss. Orbital decompression should be considered for treatment before permanent and irreversible visual loss ensues.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1177/112067211002000226DOI Listing
July 2010

Differentiating optic disc edema from optic nerve head drusen on optical coherence tomography.

Arch Ophthalmol 2009 Jan;127(1):45-9

Neuro-Ophthalmology Unit, Mason Eye Institute, University of Missouri-Columbia, Columbia, MO 65212, USA.

Objective: To assess optical coherence tomography in differentiating optic disc edema (ODE) due to papilledema and other optic neuropathies from optic nerve head drusen (ONHD).

Methods: Optical coherence tomographic images from 60 subjects (20 with ODE, 20 with ONHD, and 20 control subjects) were assessed qualitatively and quantitatively. Qualitative criteria for ODE included an elevated optic nerve head with smooth internal contour and subretinal hyporeflective space (SHYPS) with recumbent "lazy V" pattern. Optic nerve head drusen displayed a "lumpy-bumpy" internal optic nerve contour and a rapid decline in SHYPS thickness. Quantitative comparisons included retinal nerve fiber layer and SHYPS thickness.

Results: Optical coherence tomography differentiated ODE from ONHD qualitatively (sensitivity, 63%; specificity, 63%) and quantitatively (sensitivity, 80%; specificity, 90%). Respective differences in mean retinal nerve fiber layer thickness between ODE and ONHD were significant (P < .002) superiorly (206.8 vs 121.7 microm), nasally (176.3 vs 78.6 microm), inferiorly (247.2 vs 153.8 microm), and temporally (180.0 vs 85.5 microm). Respective differences in mean SHYPS thickness between ODE and ONHD were significant (P < .001) at radii of 0.75 mm (512.1 vs 274.4 microm), 1.5 mm (291.4 vs 103.0 microm), and 2.0 mm (145.5 vs 60.7 microm).

Conclusion: Optical coherence tomography can differentiate ODE from ONHD, particularly when the nasal retinal nerve fiber layer and SHYPS thickness at the 2.0-mm radius are greater than 86 microm and 127 microm, respectively.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1001/archophthalmol.2008.524DOI Listing
January 2009

Closely spaced stressful life events precede the onset of benign essential blepharospasm and hemifacial spasm.

J Neuroophthalmol 2007 Dec;27(4):275-80

From the Neuro-Ophthalmology Unit of the Mason Eye Institute, University of Missouri-Columbia, Columbia, Missouri 65212, USA.

Background: The purpose of this study was to assess the possible role of major stressful life events, complicated grief, and depression in the pathogenesis of benign essential blepharospasm (BEB) and hemifacial spasm (HFS).

Methods: This was a case-control study involving 23 participants with BEB/HFS and 23 control subjects, comparing the frequency of major stressful life events, depression on the Beck Depression Inventory-II, and complicated grief on the Inventory of Complicated Grief.

Results: There was no difference in the rate of depression or complicated grief between participants with BEB/HFS (57%) and control subjects (48%). Participants with BEB/HFS experienced a significantly (P = 0.0048) shorter time interval between two major stressful life events (median, 0.3 year) than did the control group (median, 3.0 years). The proportion of participants who had suffered two major stressful lifetime events separated by 1 year or less was significantly greater for participants with BEB/HFS than for control subjects (P = 0.0007).

Conclusions: The onset of BEB and HFS was often preceded by a major lifetime stressor. The development of these conditions was significantly related to the number of stressful life events occurring within the preceding year rather than to the total number of stressful life events. Subjects who sustain closely spaced stressful life events may be at increased risk of developing BEB and HFS.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1097/WNO.0b013e31815c4233DOI Listing
December 2007

Tetracycline delays ocular motility decline in chronic progressive external ophthalmoplegia.

Neurology 2007 Apr;68(14):1159-60

Department of Neurology, Mason Eye Institute, University of Missouri-Columbia, Columbia, MO 65212, USA.

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1212/01.wnl.0000258659.21421.b0DOI Listing
April 2007

Development and validation of a computerized expert system for evaluation of automated visual fields from the Ischemic Optic Neuropathy Decompression Trial.

BMC Ophthalmol 2006 Nov 20;6:34. Epub 2006 Nov 20.

Department of Ophthalmology, University of Rochester School of Medicine, Rochester, NY, USA.

Background: The objective of this report is to describe the methods used to develop and validate a computerized system to analyze Humphrey visual fields obtained from patients with non-arteritic anterior ischemic optic neuropathy (NAION) and enrolled in the Ischemic Optic Neuropathy Decompression Trial (IONDT). The IONDT was a multicenter study that included randomized and non-randomized patients with newly diagnosed NAION in the study eye. At baseline, randomized eyes had visual acuity of 20/64 or worse and non-randomized eyes had visual acuity of better than 20/64 or were associated with patients refusing randomization. Visual fields were measured before treatment using the Humphrey Field Analyzer with the 24-2 program, foveal threshold, and size III stimulus.

Methods: We used visual fields from 189 non-IONDT eyes with NAION to develop the computerized classification system. Six neuro-ophthalmologists ("expert panel") described definitions for visual field patterns defects using 19 visual fields representing a range of pattern defect types. The expert panel then used 120 visual fields, classified using these definitions, to refine the rules, generating revised definitions for 13 visual field pattern defects and 3 levels of severity. These definitions were incorporated into a rule-based computerized classification system run on Excel(R) software. The computerized classification system was used to categorize visual field defects for an additional 95 NAION visual fields, and the expert panel was asked to independently classify the new fields and subsequently whether they agreed with the computer classification. To account for test variability over time, we derived an adjustment factor from the pooled short term fluctuation. We examined change in defects with and without adjustment in visual fields of study participants who demonstrated a visual acuity decrease within 30 days of NAION onset (progressive NAION).

Results: Despite an agreed upon set of rules, there was not good agreement among the expert panel when their independent visual classifications were compared. A majority did concur with the computer classification for 91 of 95 visual fields. Remaining classification discrepancies could not be resolved without modifying existing definitions. Without using the adjustment factor, visual fields of 63.6% (14/22) patients with progressive NAION and no central defect, and all (7/7) patients with a paracentral defect, worsened within 30 days of NAION onset. After applying the adjustment factor, the visual fields of the same patients with no initial central defect and 5/7 of the patients with a paracentral defect were seen to worsen.

Conclusion: The IONDT developed a rule-based computerized system that consistently defines pattern and severity of visual fields of NAION patients for use in a research setting.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/1471-2415-6-34DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1685661PMC
November 2006

Facilitation as well as inhibition of the blink reflex by a visual prepulse requires intact striate cortex.

Clin Neurophysiol 2006 Oct 21;117(10):2284-91. Epub 2006 Aug 21.

Department of Psychological Sciences, 210 McAlester Hall, University of Missouri-Columbia, Columbia, MO 65211, USA.

Objective: The role of visual cortex in modulation of the human eye blink reflex was assessed.

Methods: Participants were 13 patients with unilateral striate cortex damage. Nonreflexogenic gratings were presented in their intact or blind hemifield prior to white noise or air puff blink-eliciting stimuli.

Results: Inhibition of reflex amplitude was observed at asynchronies ranging from about 120 to 600ms for visible but not invisible prepulses. Facilitation by intact-hemifield gratings was observed for (1) the latency of the acoustic blink reflex, (2) the amplitude of the disynaptic cutaneous blink reflex, R1, and (3) the latency of voluntary hand-grip reactions to the reflexogenic stimuli. These facilitatory effects were absent on trials with blind-hemifield prepulses.

Conclusions: An intact V1 is required for prepulse facilitation as well as inhibition.

Significance: These results extend a popular model of sensorimotor gating deficits in schizophrenia.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.clinph.2006.05.020DOI Listing
October 2006

Repeated intervals of high-dose corticosteroid: an overlooked therapy in multiple sclerosis.

Mo Med 2005 Jan-Feb;102(1):47-50

Department of Ophthalmology, University of Missouri-Columbia School of Medicine, USA.

The rate of conversion to multiple sclerosis is about 6% per year for five years after the first episode of optic neuritis. While the new MS agents have garnered much attention as promising agents to prevent MS relapses, an overlooked therapy is pulse high-dose corticosteroid (10 mg per kg or greater) as an intervention to delay or prevent the development of MS. Data from Optic Neuritis Treatment Trial (ONTT) and other studies underscore the need to investigate the efficacy of high-dose corticosteroid in MS.
View Article and Find Full Text PDF

Download full-text PDF

Source
April 2005

The clinical spectrum of amiodarone-associated optic neuropathy.

J Natl Med Assoc 2004 Nov;96(11):1477-91

Neuro-Opthalmology Unit, Mason Eye Institute, University of Missouri-Columbia, Columbia, MO 65212, USA.

Purpose: To describe the clinical spectrum of amiodarone-associated optic neuropathy.

Methods: Observational cases series and review.

Results: Of 55 cases, the median interval for onset of optic neuropathy was four months after initiating amiodarone; 88% occurred within 12 months. Seven (13%) patients were asymptomatic. Twenty-two (40%) patients presented with sudden visual loss, while 26 (47%) had insidious loss of vision. Visual acuity ranged from 20/15 to light perception; 10 (18%) patients had legal blindness with visual acuity of 20/200 or worse. Visual field loss was present in 91% of cases. Color vision loss was present in eight (40%) of 20 cases. Optic disc edema was present in 85% of cases, while eight (15%) patients had retrobulbar optic neuropathy, without evidence of disc edema. Optic disc edema resolved over a median time of three months. Five patients had raised intracranial pressure on lumbar puncture.

Conclusion: We were able to classify amiodarone-associated optic neuropathy into five clinical categories with respect to temporal characteristics and optic nerve appearance: insidious-onset (43%), acute-onset (28%), retrobulbar (13%), increased intracranial pressure (8%), and delayed-progressive onset (8%). Most cases of optic neuropathy commenced within 12 months of initiating amiodarone, with the median onset being four months. Over 10% of patients will have no visual symptoms at the onset. Ophthalmologic examinations within the first 12 months--and particularly within four months of initiating amiodarone--should improve early detection of amiodarone-associated optic neuropathy.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2568612PMC
November 2004

Neuroretinitis in patients with multiple sclerosis.

Ophthalmology 2004 Feb;111(2):335-40; discussion 340-1

Neuro-Ophthalmology Unit, Mason Eye Institute, University of Missouri-Columbia, Columbia, Missouri 65212, USA.

Purpose: To present a case series of three patients with neuroretinitis associated with multiple sclerosis.

Design: Retrospective, noncomparative, consecutive, interventional case series.

Participants: Thirty-five consecutive patients with neuroretinitis.

Methods: The records of 35 consecutive patients with neuroretinitis were reviewed for prior, concurrent, or subsequent development of multiple sclerosis.

Main Outcome Measures: Presentation, clinical course, and diagnosis of multiple sclerosis.

Results: Three of 35 patients (8.6%) with neuroretinitis were diagnosed with multiple sclerosis by the McDonald criteria. One of the three patients underwent brain biopsy that further confirmed multiple sclerosis. Neuroretinitis in the three patients occurred after the diagnosis of multiple sclerosis. All three patients with multiple sclerosis had been treated with interferon beta before or concurrently with the development of neuroretinitis.

Conclusions: Neuroretinitis can be an associated manifestation of multiple sclerosis. The possible association between neuroretinitis and interferon beta warrants further investigation.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/S0161-6420(03)00663-8DOI Listing
February 2004

Visual function in patients with optic nerve pallor (optic atrophy).

J Natl Med Assoc 2003 May;95(5):394-7

Department of Ophthalmology, Mason Eye Institute and Biostatistics Division of Integrated Technology Services, University of Missouri-Columbia, Columbia, Missouri 65212, USA.

This cross-sectional study assessed the relationship between the degree of optic nerve pallor (optic atrophy) and visual function. Using a set of "gold standard" stereoscopic slides, the severity of optic atrophy for 270 eyes, each having sustained a bout of optic neuropathy, was graded. Good visual acuity was found in 55/86 (64.0%) mild, 54/119 (45.4%) moderate, and 21/65 (32.3%) marked optic atrophy eyes. Good visual field was found in 6/28 (21.4%) mild, 4/43 (9.3%) moderate, and 2/28 (7.1%) marked optic atrophy eyes. Good color vision was found in 31/46 (67.4%) mild, 12/62 (19.4%) moderate, and 7/31 (22.6%) marked optic atrophy eyes. A significant rank correlation was observed between optic atrophy and visual acuity (P < 0.001; rs = 0.356), visual field (P < 0.001; rs = -0.398), and color vision (P < 0.001; rs = -0.492). As the graded severity of optic atrophy increases, the proportion of eyes with good visual function decreases. Visual field, rather than visual acuity or color vision, appears to be a better indicator of the severity of visual loss, when optic atrophy is present.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2594524PMC
May 2003

Hallucinating the past: a case of spontaneous and involuntary recall of long-term memories: perspectives on the hemispheric organization of visual memory.

J Neurol 2003 Jan;250(1):55-62

Neuro-Ophthalmology Unit, Mason Eye Institute, University of Missouri-Columbia, Columbia, Missouri 65212, USA.

This paper presents the unique case of a patient who developed palinopsias and formed visual hallucinations, representing spontaneous recall of memories from a discrete 10-year time period. The visual phenomena began shortly after the initiation of prophylactic whole-brain radiation therapy, following the removal of a metastatic adenocarcinoma in the region of the right cuneus. The most striking feature of this patient's hallucinations is the composition: memories from a discrete 10-year time period from about 30 years ago. This case provides further evidence to support the theory of a contralateral and hemispheric organization of visual memory. We propose that visual memory traces formed nearly three decades ago were spontaneously recalled in the form of hallucinations and palinopsias. It is noteworthy that the region of the brain most affected by the tumor and subsequent radiation therapy is postulated to permit perception of mental imagery. To our knowledge, no other case involving hallucination of 30-year-old memories has been reported.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s00415-003-0951-1DOI Listing
January 2003

Giant cell arteritis.

Ophthalmology 2002 Feb;109(2):220-1

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/s0161-6420(01)00963-0DOI Listing
February 2002