| OCR Text |
Show Literature Commentary Kupersmith MJ, Anderson S, Durbin M, Kardon R. Scanning laser polarimetry, but not optical coherence tomography predicts permanent visual field loss in acute nonarteritic anterior ischemic optic neuropathy. Invest Ophthalmol Vis Sci. 2013;54:5514-5519. Purpose: Scanning laser polarimetry (SLP) reveals abnormal retardance of birefringence in locations of the edematous peripapillary retinal nerve fiber layer (RNFL), which appear thickened by optical coherence tomography (OCT), in non-arteritic anterior ischemic optic neuropathy (NAION). We hypothesize that initial sector SLP RNFL abnormalities will correlate with long-term regional visual field loss due to ischemic injury. Methods: We prospectively performed automated perimetry, SLP, and high-definition OCT (HD-OCT) of the RNFL in 25 eyes with acute NAION. We grouped visual field threshold and RNFL values into Garway-Heath inferior/superior disc sectors and corresponding superior/inferior field regions. We com-pared sector SLP RNFL thickness with corresponding visual field values at presentation and at .3 months. Results: At presentation, 12 eyes had superior sector SLP reduction, 11 of which had inferior field loss. Six eyes, all with superior field loss, had inferior sector SLP reduction. No eyes had reduced OCT-derived RNFL acutely. Eyes with abnormal field regions had corresponding SLP sectors thinner (P = 0.003) than for sectors with normal field regions. During the acute phase, the SLP-derived sector correlated with presentation (r = 0.59; P = 0.02) and with .3 months after the presentation (r = 0.44; P = 0.02) corresponding superior and inferior field thresholds. Conclusions: Abnormal RNFL birefringence occurs in sec-tors corresponding to regional visual field loss during acute NAION when OCT-derived RNFL shows thickening. Since the visual field deficits show no significant recovery, SLP can be an early marker for axonal injury, which may be used to assess recovery potential at RNFL locations with respect to new treatments for acute NAION. The authors expand upon their previous work on SLP and OCT in optic disc edema of various causes (1). In the current study, they evaluated patients with acute NAION, and, not surprisingly, the OCT showed thickening of the RNFL. Meanwhile, the SLP in the acute phase showed thinning of the RNFL in areas corresponding to permanent visual field loss and normal RNFL in corresponding areas that eventually showed improvement in the visual field. Why would this be? SLP does not directly measure the actual dimensions of the RNFL. Instead, SLP depends upon the birefringence of the parallel structural organization of the RNFL. The birefringence induces a delay, called retardance, in 1 of 2 orthogonal beams of polarized light. The retardance is then used to calculate the RNFL thickness. Presumably, permanently damaged axons develop a disrupted parallel structure, which affects the calculated RNFL. The findings of this report could be extremely helpful in predicting whom to enroll in clinical trials of NAION. Clinically, it could represent a useful tool in counseling patients with acute NAION. -Michael S. Lee, MD OCT has overtaken SLP in the clinical world as the main retinal imaging tool with few ophthalmology practices using the GDx (Carl Zeiss Meditec, Dublin, CA). However, this study demonstrates a major advantage of SLP in the patient with acute NAION (and in the prior study (1) with optic neuritis). Being able to predict recovery of vision using SLP in a patient with optic nerve ischemia will be very helpful in counseling patients and evaluating future clinical trials. -Mark L. Moster, MD REFERENCE 1. Kupersmith MJ, Kardon R, Durbin M, Horne M, Shulman J. Scanning laser polarimetry reveals status of RNFL integrity in eyes with optic nerve head swelling by OCT. Invest Ophthalmol Vis Sci. 2012;53:1962-1970. Kunte H, Schmidt F, Kronenberg G, Hoffmann J, Schmidt C, Harms L, Goektas O. Olfactory dysfunction in patients with idiopathic intracranial hypertension. Neurology. 2013;81:379-382. Objective: Although accumulating evidence suggests that a malfunction of the CSF system in idiopathic intracranial hypertension (IIH) may give rise to olfactory dysfunction, little objective knowledge is available at present about the olfactory capacity of patients with this condition. Methods: Seventeen patients with IIH and 17 age- and sex-matched controls were included. The extended Sniffin' Sticks procedure was used to test odor threshold, discrim-ination, and identification (TDI). Results: Median (interquartile range) values of the compos-ite TDI score (29 [26.5-35.5] vs 35 [34-37]; P = 0.003) were reduced in patients with IIH. Furthermore, Spearman 408 Moster and Lee: J Neuro-Ophthalmol 2013; 33: 408-411 Literature Commentary Section Editors: Mark L. Moster, MD Michael S. Lee, MD Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. correlation revealed reduced TDI values in patients with a recent clinical deterioration of IIH (r = 0.66; P = 0.004). Conclusions: Our pilot study provides new evidence that olfaction is impaired in patients with IIH, especially in those who have been newly diagnosed or who have experienced a recent clinical deterioration. This study found that olfactory function was decreased in IIH patients compared with controls and that patients with acute IIH or recent worsening had the most impaired olfactory function. Although only 29% admitted to olfac-tory problems on review of systems, more were found to have deficits. Forty-one percent of IIH patients and 80% of those with acute IIH had absolute hyposmia. The mecha-nism may be similar in dysfunction of the olfactory nerve as in the optic nerve. Although we will not likely be testing smell in our patients, we may want to query our IIH patients about it. Who knows, perhaps we will find transient olfactory obscurations with change in posture! -Mark L. Moster, MD I believe that hyposmia and anosmia tend to alter the taste of food and that many individuals with altered smell add more sugar and/or salt to improve food flavor. Hyposmia may affect the ability of IIH patients to lose weight effectively, and testing olfactory function could help us counsel IIH patients regarding weight control. -Michael S. Lee, MD Raz N, Chokron S, Ben-Hur T, Levin N. Temporal reorganization to overcome monocular demyelination. Neurology. 2013;81:702-709. Objective: To identify the source of delayed visual evoked potential (VEP) latencies in the fellow eyes of patients with optic neuritis (ON) and determine whether these latencies stem from clinically silent demyelination or reflect an adaptive process for synchronization with the affected eyes. Methods: The study sample comprised 17 patients whom we followed for 12-26 months after unilateral first-ever ON diagnosis and 17 age-matched controls. To avoid confound-ing effects of axonal loss, only intact fellow eyes (except for VEPs) were included. Subjects underwent standard visual evaluation, motion perception, and static- and time-constrained stereo tasks. Assessments included VEP, optical coherence tomography, high-resolution magnetic resonance imaging, and diffusion tensor imaging. Results: We observed delayed VEP peaks (P100) in both affected and fellow eyes. However, while these were derived from prolonged time to start in the affected eyes, supporting the existence of demyelination, time to start in the fellow eyes was intact. VEP latencies in the fellow eyes could not be explained by demyelinative lesions along postchiasmal pathways (assessed by diffusion tensor imaging). Delayed peaks in fellow eyes resulted from a wider waveform, which evolved over time and occurred with a concomitant decrease in the gap in time between VEP peaks of both eyes. These changes offered a functional advantage: syn-chronization of inputs highly correlated with improved time-constrained binocular perception. Conclusion: Delayed latencies in the fellow eyes may reflect adaptive mechanisms at the cortical level that improve binocular integration over time to adjust for the damage incurred. These data provide a unique demonstration of temporal reorganization that compensates for delayed transmittal of visual information to the cortex. The authors retrospectively evaluated individuals with unilateral optic neuritis and good visual recovery. They found a delay in the P100 among affected eyes (AE) and fellow eyes (FE). In the AE, the width of the VEP waveform was similar to controls, but the time to start was significantly delayed compared to controls and FE. For the FE, the time to start was similar to controls, but the width of the waveform was wider than controls (but the width was not statistically different from the AE). The authors conclude that the widening of the waveforms in the FE may reflect an adaptive delay to more closely match the AE and provide more symmetric input from each eye. This is an interesting concept, which needs further validation. I think it would be interesting to see if this adaptive delay occurs in the FE of patients with other optic neuropathies. I also wonder how quickly this adaptation takes place. The FE showed delayed VEP time to peak at presentation compared to controls, suggesting that if the adaptation occurs, it does so in the acute phase. In this study over time, a significant increase in the time to peak in the FE did not occur (described as a "trend"), which could be explained by an adaptive change or perhaps the small number of patients. -Michael S. Lee, MD This is a very interesting study, which suggests that delayed VEP waveforms in the fellow eye of optic neuritis patients represent a central adaptation mechanism rather than a primary abnormality of the optic nerve. Although this is plausible, I don't think this study has proven the concept. First, Michael, I agree with your concern that the delayed VEP in the FE is present at the time of the optic neuritis, a bit early for central adaptation. This study also conflicts with prior papers in which the FE at onset often has a normal VEP latency. A second concern is the claim that the optic nerve in the FE is not demyelinated because the motion perception task is normal in these eyes. Although this may be correct, there is no real proof that it is, particularly with less of a delay in the FE than the AE, where motion perception is impaired. I do think that central adaptation may be a mechanism contributing to the delayed VEP in the FE. In particular, the prolonged waveform with an essentially normal N75 peak latency would support this. An interesting follow-up study would be prospective in multiple sclerosis patients who have normal baseline VEPs prior to developing unilateral Moster and Lee: J Neuro-Ophthalmol 2013; 33: 408-411 409 Literature Commentary Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. optic neuritis. We will then see VEP changes in the FE from baseline along with those in the AE. -Mark L. Moster, MD Park HY, Park YG, Cho AH, Park CK. Transneuronal retrograde degeneration of the retinal ganglion cells in patients with cerebral infarction. Ophthalmology. 2013;120:1292-1299. Purpose: The objective of this study was to determine whether transneuronal retrograde degeneration (TRD) of the retinal ganglion cells (RGCs) could be detected by optical coherence tomography (OCT) in humans with lesions other than that of the occipital lobe or visual cortex. In addition, whether laterality and severity of retinal nerve fiber layer (RNFL) damage correlated with 3 other variables was determined: laterality of hemispheric damage, arterial territory of infarct, and age of infarct. Design: Cross-sectional, case-control design. Participants: Forty-six patients with cerebral ischemic infarction diagnosed based on brain magnetic resonance imaging and 46 normal controls were enrolled. Methods: All subjects underwent a complete ophthalmic examination including OCT. Cerebral infarction was catego-rized by arterial territory: anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA). Eyes on the same side of the infarction were referred to as ipsilateral eyes, and eyes on the opposite side of the infarction were referred as contralateral eyes. Main Outcome Measures: RNFL thickness. Results: Average, superior, temporal, inferior, and nasal RNFL thicknesses were different significantly between patients with cerebral infarction and normal controls. The RNFL thicknesses were reduced significantly at the supe-rior, inferior, and nasal quadrants in the contralateral eyes and at the superior, inferior, and temporal quadrants in the ipsilateral eyes. The RNFL thickness reduction was greater in patients with PCA infarction, followed by MCA and ACA infarction, respectively. Factors related to the average RNFL thickness were time after stroke onset and infarction territory based on both univariate (P = 0.027 and P = 0.046, respectively) and multivariate (P = 0.036 and P = 0.047, respectively) analyses. Conclusions: RNFL thickness was reduced in patients with cerebral infarction, providing evidence for TRD of the RGCs. TRD was more pronounced in the nasal nerve fiber layer of the contralateral side and in the temporal nerve fiber layer of the ipsilateral side of cerebral damage. Although the classic teaching is that patients with posterior visual pathway lesions from early in life develop trans-synaptic degeneration, recent reports with OCT have shown this occurring in acquired lesions in adults. There-fore, some of the findings in the current study are to be expected. This includes eventual loss of RNFL after stroke and the predilection for temporal loss ipsilateral to and nasal loss contralateral to the side of the infarct. What is a bit surprising is the loss of RNFL after anterior cerebral artery (ACA) infarct. These patients do not have hemianopias and presumably spare visual pathway fibers. However, in this study, patients with ACA infarcts had a mean deviation on the ipsilateral and contralateral visual field (VF) almost as great as the middle cerebral artery infarcts and not much less than posterior cerebral artery infarcts. Unfortunately, the VFs are not described in this article, and there was no attempt to correlate the VF with the RNFL loss. I wonder whether the patients described with ACA infarcts really had other territories involved and had an homonymous hemianopia. If not, perhaps, the RNFL loss is not a result of the cerebral infarct but associated as part of a more diffuse vascular process. On a practical level, one must be cautious in attributing RNFL loss to a primary optic neuropathy if the patient has had a prior cerebral infarct. -Mark L. Moster, MD Transneuronal retrograde degeneration seems to occur in human and animal histologic studies, and this article supports the idea that it also happens in vivo. To me, these data bolster the contention that vision restitution therapy should not logically improve homonymous hemianopia among those individuals who suffered a stroke years ago since significant retinal ganglion cell atrophy already has taken place. -Michael S. Lee, MD Blanch RJ, Good PA, Shah P, Bishop JR, Logan A, Scott RA. Visual outcomes after blunt ocular trauma. Ophthalmology. 2013;120:1588-1591. Objective: To describe the prognosis and retinal location in patients presenting with acute traumatic maculopathy and extramacular retinal injuries. Design: Retrospective, noninterventional case series. Participants and Controls: All patients presenting with commotio retinae or sclopetaria retinae to the Birmingham Midland Eye Centre Eye Casualty from October 1, 2007, to February 23, 2011. Methods: The notes of all patients presenting with ocular trauma in the specified period were examined to identify suitable patients, and demographic and injury data were extracted. Main Outcome Measures: Outcome was assessed by visual acuity (VA). Results: For macular commotio retinae, 53 patients were identified, of whom 34 had adequate follow-up to determine the final VA. The median presenting VA was 20/40; 25 patients (74%) recovered to $20/30. The median extent of visual recovery was 0.18 logarithm of the minimum angle of resolution (logMAR). For extramacular commotio retinae, 117 patients were identified, of whom 58 had adequate follow-up to determine the final VA. The median presenting VA retinae was 20/30; 55 patients (95%) recovered to $20/30. The median extent of visual recovery was logMAR 0.076. There was 1 case of extramacular sclopetaria reti-nae. The 3 most common retinal locations of extramacular 410 Moster and Lee: J Neuro-Ophthalmol 2013; 33: 408-411 Literature Commentary Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. commotio retinae, in order of frequency, were inferotempo-ral (37%), temporal (17%), and superotemporal (17%); ,5% of cases were in a nasal location. Conclusions: This is the first report on the prognosis of acute traumatic maculopathy and extramacular commotio retinae. After macular injury, 26% of patients were left with a VA of #20/30, although the proportion with visual impair-ment is higher than this because 1) a deterioration from 20/15 to 20/30 is significant to many patients and 2) addi-tional patients are visually impaired by symptomatic para-central visual field defects, despite a normal VA. Reduced VA after extramacular commotio retinae may represent occult macular injury or previously undiagnosed visual impairment in the affected eye. Extramacular commotio occurs mostly in an inferotemporal to temporal location, consistent with direct trauma to the sclera overlying the injured retina. Recently, I overheard an ophthalmologist talking on the phone with the trauma service about a patient. He told them that the patient had commotio retinae, and he would almost certainly recover. In fact, I recall hearing the same schpiel when I was in residency, and I have repeated it myself. This article evaluated a relatively large group of patients and showed that about one-fourth with macular commotio and 3% with extramacular commotio had final visual acuities of 20/30 or worse. This prognostic informa-tion is very helpful in counseling patients with blunt ocular trauma, especially those with macular commotio. As neuro-ophthalmologists, we often encounter individ-uals who claim visual loss after an ocular injury. Looking carefully at multifocal electroretinogram and the outer retina on OCT may help detect organic loss among these patients. -Michael S. Lee, MD I agree that this is a helpful study that gives us data to back up the clinical impression that patients with commotio retinae may or may not have a reasonable degree of recovery. -Mark L. Moster, MD Czyz CN, Burns JA, Peetrie TP, Watkins JR, Cahill KV, Foster JA. Long-term botulinum toxin treatment of benign essential blepharospasm, hemifacial spasm, and Meige syndrome. Am J Ophthalmol. 2013;156:173-177. Purpose: To report the clinical success and incidence of adverse events of repetitive botulinum toxin treatment of 15 years or greater. Design: Retrospective cohort study. Methods: The study sample consisted of 37 patients from a clinical practice, 11 men and 26 women. Inclusion criteria consisted of patients treated a minimum of 15 consecutive years for facial dystonia. Seven patients had hemifacial spasm, 4 Meige syndrome, and 26 benign essential bleph-arospasm. Main outcome measures consisted of treatment efficacy and adverse events. Results: Mean treatment duration was 19.4 years (SD, 2.2) with an average of 62 (SD, 22) treatments of 70.2 (SD, 20.8) neurotoxin units. Mean duration of treatment efficacy was 127 days (SD, 37) with a 5% physician-reported minor adverse event rate and no major adverse events over each patient's clinical course. Patients reported no major and 20% incidence of minor adverse events over the treatment course. Conclusion: Results suggest that long-term botulinum toxin treatment produces clinical success in the alleviation of facial dystonia symptoms. Treatment produced a low inci-dence of major adverse events and minor adverse events. Previous studies may underreport clinical success and ove-report adverse events because of study design. This retrospective study from a single oculofacial plastic surgery group looked at patients who had been treated with botulinum toxin A for at least 15 years. By using the fourth injection (presumably beyond a "titration phase") as a base-line, Czyz et al found little change over the years, with excellent success, and a stable duration of response to each injection and a low incidence of adverse events. The authors claim that prior studies may have under-reported efficacy and overreported adverse events because of study design. However, the current study design, which only included patients treated over 15 years, would filter out patients with suboptimal efficacy or more adverse events and is biased toward better results. -Mark L. Moster, MD I hate to admit it, but I agree with you, Mark. There is tremendous selection bias since these patients are well established in a single practice. The patients from this practice with poor outcomes or more/worse adverse events might easily have left the practice before the 15-year threshold and missed the study. For instance, I had a patient whom I have injected for several years. She developed diplopia following a botulinum toxin injection earlier this year, and she later informed me that she was extremely close to finding another provider but decided to give me one more try. She might have left my practice before 15 years without my knowledge. It would have been better to see all of the data from all the patients in this practice to compare botulinum toxin dose and duration. -Michael S. Lee, MD Moster and Lee: J Neuro-Ophthalmol 2013; 33: 408-411 411 Literature Commentary Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |
