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Show Literature Commentary Moon K, Albuquerque FC, Ducruet AF, Crowley RW, McDougall CG. Resolution of cranial neuropathies following treatment of intracranial aneurysms with the pipeline embolization device. J Neurosurg. 2014;121:1085-1092. Objective: Intracranial aneurysms, especially those of the cavernous segment of the internal carotid artery (ICA), can present with cranial nerve (CN) palsies. The Pipeline Embolization Device (PED) has demonstrated safety and efficacy in the treatment of cerebral aneurysms by flow diversion, but little data exist reporting the outcomes of cranial neuropathies after treatment with the device. Methods: The prospectively maintained Barrow Neurologi-cal Institute's endovascular database was reviewed for all patients treated with the PED after presenting with 1 or more CN palsies secondary to a cerebral aneurysm since May 2011. Patient charts and digital subtraction angio-grams were reviewed to report clinical and angiographic out-comes. Only patients with clinical follow-up were included in the analysis. Results: A total of 127 patients were treated with the PED at the authors' institution after Food and Drug Adminis-tration approval. Twenty-two patients presented with cranial neuropathies, for initial inclusion in this study. Of these patients, 20 had sufficient follow-up for analysis. Cranial neuropathies included those of CN II, III, V, and VI, with presenting symptoms of diplopia, decreased visual acuity, and facial numbness and/or pain. Thirteen lesions were cavernous segment ICA aneurysms, whereas the remainder included supraclinoid and petrous segment ICA, posterior communicating artery, and basilar trunk aneurysms. At an average clinical follow-up of 9.55 months, 15 patients (75%) had resolution or significant improvement of their cranial neuropathies, and the re-maining 5 had stable symptoms. Of the 18 patients with angiographic follow-up, 12 (66.7%) demonstrated com-plete obliteration or small neck residual, whereas 6 (33.3%) had residual lesion. Patients with complete or near-complete obliteration of their lesion were signifi-cantly more likely to demonstrate symptomatic improve-ment at follow-up (P = 0.009). Two patients with persistent symptoms were eventually treated with micro-surgical bypass. Transient complications in this series included 6 extracranial hemorrhagic complications (30%) related to dual-antiplatelet therapy, all of which were managed medically. There was 1 delayed right ICA occlusion after retreatment that led to microsurgical bypass. Conclusions: Intracranial aneurysms presenting with 1 or more CN palsies show a high rate of clinical improvement after treatment with the PED. Clinical outcomes must be weighed against the risks and challenges faced with flow diverters. Further research is warranted for patients whose symptoms do not respond optimally to device placement. Intracranial aneurysms have been traditionally treated with either surgical clipping or endovascular coiling. Both techniques target the outpouching from the parent vessel. Recently, a new technique using flow diverters has been developed. It targets the endoluminal reconstruction of the parent vessel of the aneurysm (see video at http://www.ev3. net/neuro/intl/flow-diversion/embolization-device-product. htm). Currently, there are 3 types of flow diverters: pipeline embolization device (PED; Covidien, Irvine, CA), Silk flow diverter (SILK; Balt Extrusion,Montmorency, France), and the Surpass flow diverter (SURPASS; Stryker, Fremont, CA) (1). Twenty patients were retrospectively analyzed to deter-mine the cranial nerve (II, III, IV, V, and VI) outcome after treatment with the PED for an intracranial aneurysm. Portions of the internal carotid artery were involved in 18 patients (cavernous - 13; paraophthalmic/ophthalmic - 4; petrous - 1) and 1 patient each had a basilar or posterior communication artery aneurysm. In terms of symptom out-comes, 4 patients (20%) had resolution, 11 patients (55%) had improvement, and 5 patients (25%) were stable at last follow-up (range, 6-28 months with mean of 9.55 months). No patient had worsening of their symptoms with the PED. Angiographic outcome corresponded to the clinical out-come. Eighty-five percent of the patients either resolved or had improvement of their symptoms with complete or near-complete obliteration of the aneurysm compared with only 15% of the patients with angiographic evidence of a residual aneurysm. Despite the limitations of this study (few patients, short follow-up time period, lack of formal neuro-ophthalmic examination for many of the patients, and no comparator group) and the need for more studies to investigate the clinical success of flow diverters, this early study is encouraging and highlights the necessity of complete to near-complete angiographic obliteration of an aneurysm to achieve a successful clinical outcome (diplopia, visual loss). -M. Tariq Bhatti, MD I agree with you, Tariq, that this is an important early study showing the clinical benefit of PED and the ability to perform the PED along with coil embolization. The point 220 Moster and Bhatti: J Neuro-Ophthalmol 2015; 35: 220-225 Literature Commentary Section Editors: Mark L. Moster, MD M. Tariq Bhatti, MD Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. you make about lack of neuro-ophthalmologic examination is important. Most of the patients in the study had improved cranial nerve function: does that mean the abduction deficit is now 30% instead of 50%? Does that really obviate the need for the patient to occlude one eye? My practice has been to follow these patients clinically and not intervene even if there is a cranial neuropathy. I have had a few patients with significant sixth nerve paresis successfully managed with strabismus surgery, which may be less risky, particularly in an elderly patient. Considering the complication rate in this study, including one case of internal carotid artery occlusion, I think we need more support for this procedure before embracing it. -Mark L. Moster, MD REFERENCE 1. Alderazi YJ, Shastri D, Kass-Hout T, Prestigiacomo CJ, Gandhi CD. Flow diverters for intracranial aneurysms. Stroke Res Treat. 2014;2014:1-12. Popescu BF, Guo Y, Jentoft ME, Parisi JE, Lennon VA, Pittock SJ, Weinshenker BG, Wingerchuk DM, Giannini C, Metz I, Brück W, Shuster EA, Carter J, Boyd CD, Clardy SL, Cohen BA, Lucchinetti CF. Diagnostic utility of aquaporin-4 in the analysis of active demyelinating lesions. Neurology. 2015;84:148-158. Objective: To assess, in a surgical biopsy cohort of active demyelinating lesions, the diagnostic utility of aquaporin-4 (AQP4) immunohistochemistry in identifying neuromyelitis optica (NMO) or NMO spectrum disorder (NMOSD) and describe pathologic features that should prompt AQP4 immunohistochemical analysis and AQP4-immunoglobulin G (IgG) serologic testing. Methods: This was a neuropathologic cohort study of 20 surgical biopsies (19 patients: 11 cord and 9 brain), performed because of diagnostic uncertainty, interpreted as active demyelinating disease, and containing 2 or more of the following additional features: tissue vacuolation, granulocytic infiltrates, or astrocyte injury. Results: AQP4 immunoreactivity was lost in 18 biopsies and increased in 2. Immunopathologic features of the AQP4 loss cohort were myelin vacuolation (18), dystrophic astro-cytes and granulocytes (17), vascular hyalinization (16), macrophages containing glial fibrillary acid protein (GFAP)- positive debris (14), and Creutzfeldt-Peters cells (0). All 14 cases with available serum tested positive for AQP4-IgG after biopsy. Diagnosis at last follow-up was NMO/ NMOSD (15) and longitudinally extensive transverse myeli-tis (1 each relapsing and single). Immunopathologic fea-tures of the AQP4 increased cohort were macrophages containing GFAP-positive debris and granulocytes (2), mye-lin vacuolation (1), dystrophic astrocytes (1), Creutzfeldt- Peters cells (1), and vascular hyalinization (1). Diagnosis at last follow-up was multiple sclerosis (MS) and both tested AQP4-IgG seronegative after biopsy. Conclusions: AQP4 immunohistochemistry with subsequent AQP4-IgG testing has diagnostic utility in identifying cases of NMO/NMOSD. This study highlights the importance of considering NMOSD in the differential diagnosis of tume-factive brain or spinal cord lesions. AQP4-IgG testing may avert biopsy and avoid ineffective therapies if these patients are erroneously treated for MS. Neuromyelitis optica (NMO) and neuromyelitis optica spectrum disorder (NMOSD) are a group of diseases that can be a diagnostic challenge. In some situations, a biopsy specimen, of either brain or spinal cord, is needed to exclude conditions such as a neoplasm or confirm an inflammatory or demyelinating process such as multiple sclerosis (MS). The authors of this study did something very interest-ing and unique. They identified 19 patients who under-went a brain or spinal cord biopsy (total of 20 biopsies) because of the uncertainty of the clinical diagnosis and in most to exclude a neoplasm. Despite performing a biopsy, a specific diagnosis still could not be secured. The authors prospectively performed a histopathological and immuno-histochemical analysis of these cases that were diagnosed as "active inflammatory demyelination." Specifically, aquaporin-4 (AQP4) immunoreactivity was assessed to differentiate NMO/NMOSD from MS. The loss of AQP4 immunoreactivity in 18 of the biopsies was indicative of a diagnosis of NMO/NMOSD. When the serum of 14 of these patients was tested for the AQP4-immunoglobulin (AQP4-IgG), all of them were found to be positive consistent with the diagnosis of NMO/NMOSD (amazingly, in 1 patient, the final diag-nosis was confirmed 26 years after presentation!). In the final analysis, as a result of re-reviewing the biopsies in a prospective fashion and then retrospectively reviewing the clinical findings and performing AQP4-IgG, the authors were able to confirm the diagnosis of NMO/NMOSD in 15 patients, longitudinally extensive transverse myelitis in 2 patients, and MS in 2 patients. This study highlights the clinical utility of AQP4 immunohistochemistry analysis in surgical specimens with the following histological findings: active demyelination, myelin and tissue vacuolation, granulocytic inflammatory infiltrates, dystrophic astroycytes, and glial fibrillary acid protein containing macrophages. In addition, this report underscores the need to consider NMO/NMOSD in the differential diagnosis of a patient with a tumefactive brain or spinal cord lesion and to test for AQP4-IgG so as to avoid surgery and refrain from instituting inappropriate treatment. -M. Tariq Bhatti, MD For me, the take home message is that patients with mass lesions should have NMO antibody measured before biopsy. If positive, it might obviate the need for invasive surgery in some of these cases. However, I wish the authors would have provided more clinical and neuroimaging information so we would know how these patients presented. For instance, Moster and Bhatti: J Neuro-Ophthalmol 2015; 35: 220-225 221 Literature Commentary Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. were these relatively acute deficits suggestive of a demyelin-ating process with the only suggestion of tumor being the findings on MRI? -Mark L. Moster, MD Peng KP, Chen YT, Fuh JL, Tang CH, Wang SJ. Increased risk of Bell palsy in patients with migraine: a nationwide cohort study. Neurology. 2015;84:116-124. Objective: To evaluate the association between migraine and Bell palsy and to examine the effects of age, sex, migraine subtype, and comorbid risk factors for Bell palsy. Methods: This nationwide cohort study was conducted using data from the Taiwan National Health Insurance Research Database. Subjects aged 18 years or older with neurologist-diagnosed migraine from 2005 to 2009 were included. A nonheadache age- and propensity score-matched control cohort was selected for comparison. All subjects were followed until the end of 2010, death, or the occurrence of a Bell palsy event. Cox proportional hazards regression was used to calculate the adjusted hazard ratios and 95% confidence intervals (CIs) to compare the risk of Bell palsy between groups. Results: Both cohorts (n = 136,704 each) were followed for a mean of 3.2 years. During the follow-up period, 671 pa-tients (424,372 person-years) in the migraine cohort and 365 matched control subjects (438,677 person-years) were newly diagnosed with Bell palsy (incidence rates, 158.1 and 83.2/ 100,000 person-years, respectively). The adjusted hazard ratio for Bell palsy was 1.91 (95% CI, 1.68-2.17; P , 0.001). The association between migraine and Bell palsy remained significant in sensitivity analyses, and tests of interaction failed to reach significance in all subgroup analyses. Conclusions: Migraine is a previously unidentified risk factor for Bell palsy. The association between these 2 conditions suggests a linked disease mechanism, which is worthy of further exploration. Bell palsy, named after the Scottish Surgeon Charles Bell, is an idiopathic disorder of the facial nerve that was first described by Dr. Nicolaus Friedrich in the 18th century. Eighty percent of facial nerve palsies are due to Bell palsy with an incidence of 10-40 persons per 100,000 per year. The cause of Bell palsy remains somewhat obscure but may be due to reactivation of a latent herpes virus infection. However, many other causes have been associated with Bell palsy includ-ing diabetes mellitus, arterial hypertension, and pregnancy. The investigators of this study tapped into the National Heath Research Database, which contains health care information on 99% of the 23 million people of Taiwan, to determine whether there is an association between migraine and Bell palsy. Patients were stratified into 2 groups: migraine group and nonheadache (control) group. There were a total of 136,704 patients in each group after matching for age and propensity score (a method used to reduce the effects of confounding in an observational study). With a mean follow-up of 3.2 years (±1.6 years), 671 patients in the migraine group and 365 patients in the nonheadache group developed Bell palsy. The adjusted hazard ratio was 1.91 (95% confidence interval, 1.68-2.17) with a P value of ,0.001. The authors speculate that this nearly 2-fold higher risk of Bell palsy in patients with migraine may be the result of post-viral migraine related demyelination, ischemia due to migraine related vascular disorder, increased clinical aware-ness due to more frequent doctor visits, or drug-related adverse effect. The authors stated that they cannot be certain that migraine itself or the number of migraine attacks in-creases the risk of Bell palsy. Finally, given this strong asso-ciation (as strong as diabetes mellitus and arterial hypertension), the authors suggest a common mechanism is at play between migraine and Bell palsy. The journal NEUROLOGY felt this was such an important article that an accompanying editorial was published (1). -M. Tariq Bhatti, MD This study is interesting, even if there is no obvious way of linking a risk for Bell palsy with migraine. However, given that this association was derived from a database raises some issues that were partially addressed in the accompa-nying editorial. We are not provided any detailed clinical information. The fact that they used a migraine cohort diagnosed by a neurologist might increase the likelihood of a diagnosis of Bell palsy. Additionally, patients with mild migraine may have been excluded because they might not seek attention or have a diagnosis listed in the database. -Mark L. Moster, MD REFERENCE 1. Silberstein DS, Silvestrini M. Does migraine produce facial palsy? For whom the Bell tolls. Neurology. 2015;84:108-109. Huisingh C, McGwin G, Wood J, Owsley C. The driving visual field and a history of motor vehicle collision involvement in older drivers: a population-based examination. Invest Ophthalmol Vis Sci. 2015;56:132-138. Purpose: We designed a visual field test focused on the field used while driving to examine associations between field impairment and motor vehicle collision involvement in 2,000 drivers aged 70 years or older. Methods: The "driving visual field test" involved measuring light sensitivity for 20 targets in each eye, extending 158 superiorly, 308 inferiorly, 608 temporally, and 308 nasally. The target locations were selected on the basis that they fell within the field region used when viewing through the windshield of a vehicle or viewing the dashboard while driv-ing. Monocular fields were combined into a binocular field based on the more sensitive point from each eye. Severe impairment in the overall field or a region was defined as average sensitivity in the lowest quartile of sensitivity. 222 Moster and Bhatti: J Neuro-Ophthalmol 2015; 35: 220-225 Literature Commentary Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. At-fault collision involvement for 5 years before enrollment was obtained from state records. Poisson regression was used to calculate crude and adjusted rate ratios (RRs) examining the association between field impairment and at-fault collision involvement. Results: Drivers with severe binocular field impairment in the overall driving visual field had a 40% increased rate of at-fault collision involvement (RR, 1.40; 95% confidence interval [CI], 1.07-1.83). Impairment in the lower and left fields was associated with elevated collision rates (RR, 1.40; 95% CI, 1.07-1.82 and RR, 1.49; 95% CI, 1.15- 1.92, respectively), whereas impairment in the upper and right field regions was not. Conclusions: Results suggest that older drivers with severe impairment in the lower or left region of the driving visual field are more likely to have a history of at-fault collision involvement. Previous studies of visual field (VF) defects in relation to motor vehicle collisions (MVCs) have had varying results. Some of the differences relate to the method of testing (monocular vs binocular, threshold vs screening). Moreover, the vision requirements related to driving vary from state to state in the United States and from country to country. The range in the United States is from no rules related to visual field testing to up to 140 degrees of binocular visual field required. The current study correlated VF results in 2,000 individuals over the age of 70 years with their past 5-year driving record, looking at MVCs where the person was considered to be at-fault. The findings were that VF defects were associated with a 40% increased risk of at-fault collision involvement. The locations of VF defect associated with increased risk included the horizontal meridian, lower VF, and left VF but not the upper and right VF. This study is more useful than many previous studies. First, the authors developed a threshold visual field based on the actual parts of the VF used in driving and eliminated points that were not involved. This improved the validity of the test results. Second, they adjusted for confounding variables, including age, sex, race, visual acuity, contrast sensitivity, mental status (Mini Mental Status Examination), visual processing speed, and the number of comorbidities. Third, it was done in Alabama where drivers do not undergo repeat visual testing after receiving their initial driving license, and despite the requirement for 110 degrees of VF along the horizontal meridian, this is not tested for routinely. One limitation of this study relates to the issue of comorbidities. For instance, if one patient has hypertension but another has had a stroke with hemiparesis those are not equal in effect and would have an impact on the results. Another limitation pointed out by the authors is that subjects with VF defects may have self-selected not to drive, which would contribute to underestimating the risk of MVCs in this study. An interesting finding is that the impairment in the left VF was more important than the right VF. One wonders if this is related to oncoming traffic and whether the results might be the opposite in countries where one drives on the left side of the road. Finally, it is very surprising that 14% of this randomly selected sample at an at-fault MVC in the past 5 years. Whether this is really higher than younger Alabama subjects is not available from this study but raises some very interesting questions. Studies like this hopefully will lead to improved testing of the VF to assess for driving safety and more useful guidelines. -Mark L. Moster, MD I have always had questions in my mind regarding the best visual field test to determine a patient's ability to safely drive. I am curious to see if and how various states will change their current visual field requirements based on this more "real-world" visual field test and at what collision rate threshold will a visual field defect be acceptable? Will it be 20%, 30%, 40%, etc? Also, based on this study, it seems that it is not just the overall visual field impairment that matters but rather the location of the visual field defect that correlates with the risk of an MVC. -M. Tariq Bhatti, MD Leon M, Hutchinson AK, Lenhart PD, Lambert SR. The cost-effectiveness of different strategies to evaluate optic disk drusen in children. J AAPOS. 2014;18:449-452. Purpose: To compare the costs of diagnostic workup for optic disc drusen where ophthalmic ultrasound was per-formed before imaging and invasive studies with those where ophthalmic ultrasound was performed after such studies. Methods: The medical records of patients at the age of 18 years evaluated at a tertiary referral center between 2007 and 2012 for "swollen" optic nerves were retrospectively reviewed. The main outcome measure was cost of diagnos-tic workup according to Georgia Medicaid global reimburse-ment rates. Results: A total of 46 children with a B-scan ultrasound- confirmed diagnosis of calcified optic disc drusen were included. Neuroimaging was performed in 23 patients, of whom 20 had the study before ophthalmic ultrasound. The mean cost of evaluations for patients undergoing ancil-lary testing before ophthalmic ultrasound was $1,173; for those undergoing ancillary testing after, $305. Conclusions: Because optic disc drusen can mimic the appearance of papilledema, it is more cost effective to perform ophthalmic ultrasonography before neuroimaging, especially when the patient is asymptomatic. If ophthalmic ultrasonography confirms the presence of drusen, it is more cost effective to reassess the clinical picture before pro-ceeding with further tests. This study found that when pediatric patients with calcified optic disc drusen found on ultrasound (US) had the US Moster and Bhatti: J Neuro-Ophthalmol 2015; 35: 220-225 223 Literature Commentary Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. before other studies (e.g., magnetic resonance imaging, lumbar puncture), patient care costs were much lower. Possible reasons the authors provide for why neuroimaging and/or lumbar puncture were ordered before US include lack of access to US, shortage of staff trained to detect drusen, and medicolegal reasons. The study findings show cost-effectiveness is initially obtaining an US examination, and I believe that the savings are underestimated. First, these investigators used Georgia Medicaid reimbursement rates for the calculations, which are likely lower than private insurers. Additionally, they used an LP cost of $107 which I doubt includes all the costs for analysis of cerebrospinal fluid. Nevertheless, the results of this report are no surprise, and I think the authors make reasonable recommendations to perform the US first if the suspicion of elevation of intracranial pressure based on clinical history and fundu-scopic examination is low. One can always proceed with further workup after US if there is still suspicion of elevated intracranial pressure, as was done in 3 patients in this study. -Mark L. Moster, MD I agree that the results of this study were predictable and not surprising. No doubt that in some cases, it can be very difficult to differential true papilledema from pseudopapilledema due to buried optic disc drusen based solely on funduscopic examination. My practice has been to obtain B-scan ultrasonography, intravenous fluores-cein angiography (looking for disc leakage associated with papilledema), or fundus autofluorescence imaging before ordering neuroimaging. However, I think it is important to remember that there is no reason that a patient cannot have both papilledema and buried disc drusen. We are not told exactly why the 20 patients underwent B-scan ultrasonography only after other studies were done. As Mark has pointed out and the authors state: "Possible reasons for physicians ordering neuroimaging and other studies before ophthalmic ultrasound include lack of access to ophthalmic ultrasonography, shortage of ancil-lary staff trained to detect optic nerve head drusen, and a desire to rule out serious intracranial pathology for med-icolegal reasons." It would be interesting to assess the thought process of the clinicians who initially evaluated these 20 patients. The authors discuss the possibility of optical coher-ence tomography (OCT) as a better test for detecting disc drusen than B-scan ultrasonography. However, I would temper that enthusiasm based on the recent study by Kukarni et al (1) that showed spectral domain OCT could not reliably differentiate mild papilledema from buried disc drusen. -M. Tariq Bhatti, MD REFERENCE 1. Kulkarni KM, Pasol J, Rosa PR, Lam BL. Differentiating mild papilledema and buried optic nerve head drusen using spectral domain optical coherence tomography. Ophthalmology. 2014;121:959-963. Gilden D, White T, Khmeleva N, Heintzman A, Choe A, Boyer PJ, Grose C, Carpenter JE, Rempel A, Bos N, Kandasamy B, Lear-Kaul K, Holmes DB, Bennett JL, Cohrs RJ, Mahalingam R, Mandava N, Eberhart CG, Bockelman B, Poppiti RJ, Tamhankar MA, Fogt F, Amato M, Wood E, Durairaj V, Rasmussen S, Petursdottir V, Pollak L, Mendlovic S, Chatelain D, Keyvani K, Brueck W, Nagel MA. Prevalence and distribution of VZV in temporal arteries of patients with giant cell arteritis. Neurology. 2015. pii: 10.1212/WNL.0000000000001409. Epub ahead of print. Objective: Varicella-zoster virus (VZV) infection may trigger the inflammatory cascade that characterizes giant cell arteritis (GCA). Methods: Formalin-fixed, paraffin-embedded GCA-posi-tive temporal artery (TA) biopsies (50 sections/TA) including adjacent skeletal muscle and normal TAs ob-tained postmortem from subjects .50 years were examined by immunohistochemistry for presence and distribution of VZV antigen and by ultrastructural exami-nation for virions. Adjacent regions were examined by hematoxylin and eosin staining. VZV antigen-positive slides were analyzed by polymerase chain reaction for VZV DNA. Results: VZV antigen was found in 61 of 82 GCA-positive TAs (74%) compared with 1 of 13 normal TAs (8%) (P , 0.0001; relative risk 9.67; 95% confidence interval, 1.46- 63.69). Most GCA-positive TAs contained viral antigen in skip areas. VZV antigen was present mostly in adventitia, followed by media and intima. VZV antigen was found in 12 of 32 skeletal muscles (38%) adjacent to VZV antigen- positive TAs. Despite formalin fixation, VZV DNA was de-tected in 18 of 45 GCA-positive VZV antigen-positive TAs (40%), in 6 of 10 VZV antigen-positive skeletal muscles (60%), and in 1 VZV antigen-positive normal TA. VZVs were found in a GCA-positive TA. In sections adjacent to those containing VZV, GCA pathology was seen in 89% of GCA-positive TAs but in none of 18 adjacent sections from normal TAs. Conclusions: Most GCA-positive TAs contained VZV in skip areas that correlated with adjacent GCA pathology, supporting the hypothesis that VZV triggers GCA immu-nopathology. Antiviral treatment may confer additional benefit to patients with GCA treated with corticosteroids, although the optimal antiviral regimen remains to be determined. This is a very intriguing article demonstrating evidence that varicella-zoster virus (VZV) triggers giant cell arteritis (GCA). As noted, not all patients had evidence of VZV, suggesting that VZV may be one of numerous causes of GCA. The study was done in specimens that were 224 Moster and Bhatti: J Neuro-Ophthalmol 2015; 35: 220-225 Literature Commentary Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. deidentified, so no information is available regarding clinical history of zoster, medications, or zoster vaccination. The authors propose that the spread of VZV is transxonal to arteries, infecting the adventitia with subsequent transmural involvement, and primarily affecting the temporal artery. They do not speculate on how the disease spreads to all the other arteries typically involved in GCA. Presumably, there would be a systemic inflammatory response that affects arteries remote from the temporal artery. The authors advocate addition of antiviral treatment with IV acyclovir to corticosteroids in GCA patients and suggest that it may shorten the length of treatment with steroids. This is likely a premature recommendation but one certainly worth further study. -Mark L. Moster, MD I recall several years ago, the theory of VZV as a possible underlying etiology of GCA and whispers of treating patients with antiviral medication. This study certainly resurrects that concept, and no doubt warrants further studies of antiviral therapy in a randomized controlled design. However, until these clinical studies can be performed, corticosteroids remain the standard of care for the treatment of GCA! -M. Tariq Bhatti, MD Moster and Bhatti: J Neuro-Ophthalmol 2015; 35: 220-225 225 Literature Commentary Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |
