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HISTORICAL NEUROLOGY: How did stroke become of interest to neurologists?: A slow 19th century saga
HISTORICAL NEUROLOGY: How did stroke become of interest to neurologists?: A slow 19th century saga
Paciaroni and Bogousslavsky (1 September 2009)
[Abstract][Full text][PDF]
How did stroke become of interest to neurologists?: A slow 19th century saga How did stroke become of interest to neurologists?: A slow 19th century saga
20 November 2009
Helio A. Teive, Federal University of Parana Rua General Carneiro 1103/102, Curitiba, PR 80060-150 Brazil, Renato P. Munhoz
Drs. Paciaroni and Bogousslavsky present an excellent historical review of the growing interest of stroke among neurologists sparked by the development of clinical-topographical correlation studies. These early studies were conducted by Dejérine, Marie, and particularly Foix. [1]
The authors stated that stroke was never a field of critical interest in the Salpętričre and Pitié Schools when Vulpian and Charcot were the leading figures. However, one of Charcot`s major interests in this area was brain hemorrhage, particularly describing the well known aneurysms of Charcot-Bouchard. [2]
In addition, three of Charcot's pupils studied stroke including Henri Duret who performed the first modern anatomical studies of the cerebral arteries. [3] The study of lacunes was one of the most important contributions of Pierre Marie to the field of neurology. [4] Charles Foix, a pupil of Marie, also developed seminal works on brain infarction. [5]
Even though stroke was not the main interest of Charcot´s group, their contributions in this area were relevant.
References
1. Paciaroni M, Bogousslavsky J. How did stroke become of interest to neurologists? A slow 19th century saga. Neurology 2009;73:724-728.
2. 2. Charcot JM, Bouchard C. Nouvelles recherchers sur la pathogenie de l´hémorragie cerébrale. Arch Physiol Norm Pathol 1868;1:110-127,643-665,725-734.
3.Duret H. Recherches anatomiques sur la circulation de l´encéphale. Arch Physiol Norm Pathol 1874;1:60-91,316-353,664-693,919-957.
4. Marie P. Des foyers lacunaires de désintégration et de différents autres états cavitaries du cerveau. Rev Med 1901;31:281-298.
Disclosures: Dr. Teive is a member of editorial board of the Arquivos de Neuropsiquiatria (Brazilian Journal of Neurology and Psychiatry) and Parkinsonism and Related Disorders Journals. Dr. Munhoz reports no disclosures.
How did stroke become of interest to neurologists?: A slow 19th century saga Reply from the authors
20 November 2009
Maurizio Paciaroni, University of Perugia Stroke Unit, Santa Maria della Misercordia Hospital, University of Perugia, Perugia, Italy, Julien Bogousslavsky
mpaciaroni{at}med.unipg.it Maurizio Paciaroni, et al.
We thanks Drs. Teive and Munhoz for their interest in our article. [1] We agree that Charcot and his pupils contributed to relevant studies of stroke and we are addressing this topic. [5] Charcot and his group presented several works dealing with cerebrovascular disease, including histological studies of brain “softening”, paraneoplastic infarction, and consequences of stroke including arthropathies, vegetative changes, contractures, and abnormal movements.
Brain localization, one of Charcot’s major neurological topics, was also largely based on stroke case studies. Charcot’s work on stroke is poorly recognized because his interest focused on other fields such as hysteria and hypnotism.
Furthermore, after the mid-1860s, Charcot and his immediate followers no longer made significant contributions to stroke. This was particularly striking during the last decade of Charcot’s life (1883-1893), since the topic of stroke is not represented within the scientific literature of his group.
Reference
5. Bogousslavsky J, Paciaroni M. Did Jean-Martin Charcot contribute to stroke? Cerebrovasc Dis (In press).
Disclosure: Dr. Paciaroni has served on the speakers' bureaus of Sanofi Aventis and Boehringer Ingelheim. Dr. Bogousslavsky serves as an editorial board member of Clinical Neurology and Neurosurgery, International Journal of Neural System, BMC Neuroscience, as chief editor of European Neurology, Frontier in Neurology and Neuroscience, and as guest editor of Cerebrovascular Diseases.
ARTICLES: Microstructural white matter changes in metabolic syndrome: A diffusion tensor imaging study
Segura et al. (11 August 2009)
[Abstract][Full text][PDF]
Microstructural white matter changes in metabolic syndrome: A diffusion tensor imaging... Microstructural white matter changes in metabolic syndrome: A diffusion tensor imaging study
24 November 2009
Heikki Savolainen, Department of Occupational Safety & Health POB 536, FIN-33101 Tampere, Finland
Segura et al. presented an elegant study on CNS white matter changes in metabolic syndrome. [1] The syndrome is defined by inappropriate control of blood glucose so its metabolic consequences can be compared to diabetes. Diabetes is associated with peripheral polyneuropathy with loss of principal myelin protein species in Wallerian degeneration. [2] This may be due to the excessive glucose or to its metabolites including methylglyoxal, a bicarboxylic compound that can cross-link polypeptides. [3] The end metabolite of methylglyoxal is D-lactate, which can be considered the biological marker. [4]
References
1. Segura B, Jurado MA, Freixenet N, et al. Micro- structural white matter changes in metabolic syndrome. Neurology 2009;73:438-444.
2. Palo J, Savolainen H, Haltia M. Proteins of peripheral nerve myelin in diabetic neuropathy. J Neurol Sci 1972;16:193-119.
3. Chellan P, Nagarajah RH. Protein crosslinking by the Maillard reaction. Dicarbonyl-derived imidazolium crosslinks in aging and diabetes. Arch Biochem Biophys 1999;368:98-108.
4. Talasniemi JP, Pennanen S, Savolainen H, et al. Assay of D-lactate in diabetic plasma and urine. Clin Biochem 2008;41:1099-1103.
Disclosure: The author reports no disclosures.
Microstructural white matter changes in metabolic syndrome: A diffusion tensor imaging... Reply from the author
24 November 2009
Maria A. Jurado, University of Barcelona Passeig de la Vall d’Hebron 171, 08035, Barcelona, Spain
We thank Dr. Savolainen for the comments on our article. Diabetes is associated with peripheral polyneuropathy but this manifestation is usually a late complication. The sample we studied was free of problems associated with metabolic syndrome. We also limited our study to assess the silent manifestation of metabolic syndrome in CNS but not the peripheral nervous system. In future studies, the determination of D-lactate in our sample and the correlation analysis with white matter change indicators will be valuable.
Disclosure: The author reports no disclosures.
RESIDENT AND FELLOW SECTION: Teaching NeuroImages: Reversible ectropion in myasthenia gravis
Solé et al. (20 October 2009)
[Full text][PDF]
Teaching NeuroImages: Reversible ectropion in myasthenia gravis Teaching NeuroImages: Reversible ectropion in myasthenia gravis
24 November 2009
Gregory Y. Chang, University of California at Irvine 101 The City Drive South, Building 26, Suite 1003 Orange, CA 92868
Sole et al. utilized different camera angles to document a reversible left ectropion in a patient with myasthenia gravis before and after a neostigmine. [1]
They documented the left ectropion from the camera angle position to the patient’s left and above horizontal, which highlighted the reddish lower lid eversion. After the neostigmine, the camera position was moved to the patient’s right and below the horizontal level. In addition, the left eye is hypertropic. This new camera angle and repositioning of the head is not likely to demonstrate any objective changes in the left lower lid eversion. The noted improvement may be the result of the change in camera angle.
The most striking feature of the exposed red lower lid has been further deemphasized by reduction of the red hue perhaps due to the use of digital imaging software as mentioned in the authors’ acknowledgement. Finally, the patient looking down at the camera could be misinterpreted as ptosis, which may be confusing to readers.
I agree with the authors’ conclusion despite the different camera angles. I am a neurology dinosaur—a bipod trained before MRI--[2]and applaud the importance of close clinical observation. In this era of instant visual diagnosis, presentation of source imagery should be consistent with minimal alteration of the original image to document a transient physical finding. This will minimize roaring and rumbling from dinosaur caves!
References
1. Sole G, Perez F, Ferrer X. Teaching NeuroImages: Reversible ectropion in myasthenia gravis. Neurology 2009;73:e83.
2. Pascuzzi R. A dinosaur roars. Assessing clinical skills in residency. Neurology 2009;73:826-827.
Disclosure: The author reports no disclsoures.
Teaching NeuroImages: Reversible ectropion in myasthenia gravis Reply from the authors
24 November 2009
Guilhem Solé, Centre de référence des maladies neuromusculaires et service de neurologie CHU de Bordeaux, avenue de Magellan, 33604 Pessac Cedex, Xavier Ferrer
guilhem.sole{at}chu-bordeaux.fr Guilhem Solé, et al.
We are pleased that Dr. Chang enjoyed reading our article. [1]
We agree that the camera angle is slightly different because we actually work in prehistoric conditions! We did not have a stereotactic frame to immobilize the head of the patient during the injection of neostigmine. Nevertheless, we confirm that the regression of ectropion was evident regardless of the camera angle and there was no correction of ectropion by digital imaging software. This software was only used to crop the photo.
We appreciate Dr. Chang’s interpretation and would like to note that some dinosaurs emerged from caves to conquer the sky as birds. [3]
Reference
3. Sereno PC. The evolution of dinosaurs. Science 1999;284:2137-2147.
Dr. Solé received nonindustry-sponsored funding for travel. Dr. Ferrer reports no disclosures.
CLINICAL/SCIENTIFIC NOTES: SEVERE CARDIAC FAILURE IN A PATIENT WITH MULTIPLE SCLEROSIS FOLLOWING LOW-DOSE MITOXANTRONE TREATMENT
Dörr et al. (22 September 2009)
[Full text][PDF]
SEVERE CARDIAC FAILURE IN A PATIENT WITH MULTIPLE SCLEROSIS FOLLOWING LOW-DOSE MITOXANTRONE... SEVERE CARDIAC FAILURE IN A PATIENT WITH MS FOLLOWING LOW-DOSE MITOXANTRONE TREATMENT
20 November 2009
Joep Killestein, VU Medical Center, Dept of Neurology PO Box 7057, 1007MB Amsterdam, The Netherlands, Marieke L. van der Meer, Josien C. Regelink, Peter C. Huijgens, Chris H. Polman
Mitoxantrone (MiTX) reduces relapse frequency and MRI evidence of disease activity in relapse-onset MS. MiTX is a toxic agent that must be carefully administered to reduce the likelihood of bone marrow suppression, opportunistic infection, leukemia, and cardiomyopathy. The risk of cardiomyopathy is generally assumed to be dose dependent. Dörr et al. suggest that toxic cardiomyopathy may occur after a relatively low dose (i.e., two infusions) given very early after treatment is initiated. [1] This challenges the assumption that MiTX given below a certain cumulative dose can be considered safe regarding the risk of heart failure.
We present a case of severe heart failure that occurred 26 months after the final (sixth) infusion of MiTX in a 48-year-old woman with RRMS. The total cumulative dose had only been 72 mg/m2 (12 mg/m2 body surface area per infusion at three months intervals). The patient had baseline and follow-up echocardiograms that were all normal (left ventricular ejection fraction [LVEF] 58% at baseline, 59% after the second [month 6] and 60% after the fourth infusion [month 12 after the start of treatment]). She did not have additional echocardiograms as no further infusions were scheduled after the eighteenth month. More than two years after her last MiTX infusion, she visited a cardiologist because of progressive fatigue and edema in both legs. A severe dilated cardiomyopathy was diagnosed (LVEF 20%).
This is an unusual report of severe delayed heart failure following a low cumulative dose of mitoxantrone in MS. Cases of severe delayed cardiac failure were described after cumulative doses of at least 144 mg/m2. [2] Our findings support the FDA safety notices of July 2008, [3] which recommend that all MS patients receiving MiTX should undergo reevaluation of LVEF before receipt of each dose of MiTX. In addition, patients should receive a yearly quantitative LVEF evaluation after stopping MiTX to monitor late-occurring cardiotoxicity.
References
1. Dörr J, Bitsch A, Schmailzl KJ, et al. Severe cardiac failure in a patient with multiple sclerosis following low-dose mitoxantrone treatment. Neurology 2009;73:991-993.
2. Goffette S, van Pesch V, Vanoverschelde JL, Morandini E, Sindic CJ. Severe delayed heart failure in three multiple sclerosis patients previously treated with mitoxantrone. J Neurol 2005;252:1217-1222.
3. FDA MedWatch Safety Alert. Mitoxantrone Hydrochloride (marketed as Novantrone and generics). July 29, 2008. Available at: http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm092708.htm. Accessed October 15, 2009.
Disclosure: Dr Killestein received research support from Teva, Genzyme, Novartis, Merck Serono, Biogen Idec and Bayer Schering and has received research support paid to his institution. Dr van der Meer, Dr Regelink and Prof Huijgens report no disclosures. Dr. Polman has served on advisory or data monitoring committees of Actelion, Biogen Idec, Bayer Schering, Teva, Merck-Serono, Novartis, GlaxoSmithKline, UCB, Roche and Antisense Therapeutics; has received speaker honoraria from Biogen Idec, Schering AG, Novartis, and Teva; receives research support from Biogen Idec, Bayer Schering, GlaxoSmithKline, Novartis, UCB, Merck-Serono, Teva, the European Community [NABINMS contract 018926 (PI)], and the Dutch Multiple Sclerosis Society [02/358b (PI), 05/358c (PI)]; and serves as an editorial board member of Lancet Neurology and Multiple Sclerosis.
SEVERE CARDIAC FAILURE IN A PATIENT WITH MULTIPLE SCLEROSIS FOLLOWING LOW-DOSE MITOXANTRONE... Reply from the author
20 November 2009
Jan Dörr, NeuroCure Clinical Research Center, Charite Universitätsmedizin Berlin Chariteplatz 1, 10117 Berlin, Germany
Killestein et al. report another case of severe cardiac failure in a patient with MS after the relatively low mitoxantrone dose of 72 mg/m2. The fact that the delayed type cardiac failure in this patient occurred more than two years after termination of low-dose mitoxantrone treatment is uncommon for mitoxantrone-mediated cardiotoxicity. Because mitoxantrone is still an important therapeutic option in severe and progressive MS courses, alternative causes of cardiac failure should be sufficiently excluded before mitoxantrone is considered as an underlying cause. This report further challenges the assumption that a safe cumulative mitoxantrone dose exists. In addition, it underscores the importance of regular cardiologic follow-up examinations in mitoxantrone-treated patients and the need for reliable markers for patients at risk. [4]
Reference
4. Cotte S, von Ahsen N, Kruse N, et al. ABC-transporter gene-polymorphisms are potential pharmacogenetic markers for mitoxantrone response in multiple sclerosis. Brain 2009;132:2517-2530.
Disclosure: The author reports no disclosures.
ARTICLES: Randomized, controlled trial of telcagepant for the acute treatment of migraine
Connor et al. (22 September 2009)
[Abstract][Full text][PDF]
Randomized, controlled trial of telcagepant for the acute treatment of migraine Randomized, controlled trial of telcagepant for the acute treatment of migraine
20 November 2009
Rachel Nardin, Cambridge Health Alliance 1493 Cambridge St. Macht 420, Cambridge MA 02139
Connor et al. report that the use of 150 mg of telcagepant results in pain relief at 2 hours in 54% of migraine patients compared to 33% of patients achieving this endpoint with placebo. [1] This industry-sponsored trial written by industry employees raises serious concerns.
Triptans are the standard care for moderate to severe migraine. Sumatriptan 50 mg, now available as a generic, results in pain relief at 2 hours in 50% to 59% of migraine patients compared to 17% to 26% for placebo. [2] The relevant question for patients and physicians is whether telcagepant offers any advantage over sumatriptan.
The authors justify comparing telcagepant to placebo—rather than to active treatment— because it may be used in patients with coronary artery or cerebrovascular disease, in whom triptans are contraindicated. However, if this is the population of interest for telcagepant, it should be tested in this population.
There is sufficient preliminary data supporting the superiority of telcagepant to placebo. A placebo-controlled trial in the population of patients eligible for triptan treatment before a trial in the clinically relevant population of migraineurs with coronary artery and cerebrovascular disease was not needed.[3]
The objective of this trial appears to be to bolster FDA drug approval and marketing efforts.
References
1. Connor KM, Shapiro RE, Diener H-C et al. Randomized, controlled trial of telcagepant for the acute treatment of migraine. Neurology 2009;73:970-977.
3. Tepper SJ, Cleves C. Telcagepant, a calcitonin gene-related peptide antagonist for the treatment of migraine. Curr Opin Investig Drugs 2009;10:711-720.
Disclosure: Dr. Nardin serves on the editorial board of Muscle & Nerve; has received honoraria from academic institutions for giving grand rounds; and receives royalties from UpToDate.
Randomized, controlled trial of telcagepant for the acute treatment of migraine Reply from the authors
20 November 2009
Tony W. Ho, Merck Research Laboratories UG 4C-18, PO Box 1000, North Wales, PA 19454-1099, Kathryn M. Connor, Robert E. Shapiro, Hans-Christoph Diener, Sylvia Lucas, James Kost, Xiaoyin Fan, Kaiyin Fei, Christopher Assaid, Christopher Lines
Dr. Nardin questions the value of our second pivotal trial of telcagepant [1], stating that there were already sufficient data to support the superiority of telcagepant to placebo.
The regulatory approval process for new migraine medicines is rigorous and requires substantial evidence of efficacy and safety. This is usually achieved through conducting two well-controlled pivotal trials. At an alpha=0.05 level, there is a 1 in 20 risk of a false positive efficacy result within one trial. With two independent pivotal studies, the probability of a false positive in both studies is 1 in 400. Dr. Nardin states that “The publication of this trial raises serious concerns.” On the contrary, it would be a serious cause for concern if we had failed to publish it. In addition, the data was considered of high enough priority to publish.
Dr. Nardin mentions a possible study of patients with coronary artery or cerebrovascular disease. This study has recently been completed [4] and the results will be published. In addition to benefiting cardiovascular disease patients, CGRP receptor antagonists may benefit those intolerant of or poorly responsive to existing treatments due to the antagonists’ alternative mechanism.
Recent data suggest that only 19% of migraineurs use triptans over a one-year period. [5] This figure is low considering that 17% use opioid or barbiturate drugs, [5] which can result in migraine chronification [6] and may be associated with abuse/dependence concerns. These observations confirm that there are unmet treatment needs. CGRP receptor antagonists represent another choice for migraine sufferers.
Dr. Nardin also questions the sponsorship and authorship of our study. Novel medicines are developed by pharmaceutical companies in collaboration with academic experts and clinical investigators. Optimally, the process of developing pharmaceuticals that meet important medical needs should be guided by the clinical experiences of health care providers to help clarify those needs on behalf of patients.
Reasonable compensation of physicians for their efforts and expertise in drug development is appropriate as long as disclosure is transparent as was the case for our paper. We believe that a collaborative approach to developing new medicines serves the interests of patients.
References
4. Treatment of Migraine in Patients With Stable Vascular Disease. NCT00662818. Available at: http://www.clinicaltrials.gov/. Access October 18, 2009.
5. Bigal ME, Borucho S, Serrano D, Lipton RB. The acute treatment of episodic and chronic migraine in the USA. Cephalalgia 2009;29:891-897.
6. Bigal ME, Lipton RB. Excessive acute migraine medication use and migraine progression. Neurology 2008;71:1821-1828.
Disclosures: Drs. Connor, Kost, Fan, Fei, Assaid, Lines, and Ho are employees of, and own stock and/or stock options in, Merck & Co., Inc. Dr. Shapiro serves or has served on scientific advisory boards for, and received honoraria and funding for travel from Merck & Co, Inc., MAP Pharmaceuticals, and NuPathe; and has received research support from Merck & Co, Inc. and the NIH [NHLBI #R01HL71944 (Co-Investigator)]. Dr. Diener has received honoraria for participation in clinical trials, contribution to advisory boards or lectures from Addex Pharma, Allergan, Almirall, AstraZeneca, Bayer Vital, Berlin Chemie, Coherex Medical, CoLucid, Böhringer Ingelheim, Bristol-Myers Squibb, GlaxoSmithKline, Grünenthal, Janssen-Cilag, Lilly, La Roche, 3M Medica , Minster, MSD, Novartis, Johnson & Johnson, Pierre Fabre, Pfizer, Schaper and Brümmer, SanofiAventis, and Weber & Weber; has received research support from Allergan, Almirall, AstraZeneca, Bayer, GSK, Janssen-Cilag, and Pfizer. Headache research at the Department of Neurology in Essen is supported by the German Research Council (DFG), the German Ministry of Education and Research (BMBF), and the European Union. Dr. Lucas has served on scientific advisory boards for GlaxoSmithKline, Merck & Co. Inc., and Bayer (formerly Berlex); has received honoraria from Allergan, GlaxoSmithKline, Merck & Co. Inc., EMD Serono, Biogen Idec, Pfizer, Endo, OMP, Teva Neuroscience, the National Multiple Sclerosis Society, and Headache Cooperative of the Pacific; has served on the speaker's bureaus of GlaxoSmithKline, Merck & Co. Inc., EMD Serono, Biogen Idec, and Pfizer; has received research support from GlaxoSmithKline, Merck & Co. Inc., Allergan, Nupathe, MAP, Biogen Idec, Sanofi-Aventis, and AGA.
ARTICLES: Epilepsy in children with infantile thiamine deficiency
Fattal-Valevski et al. (15 September 2009)
[Abstract][Full text][PDF]
Epilepsy in children with infantile thiamine deficiency Reply from the author
24 November 2009
Aviva Fatal-Valevski, Tel Aviv University Pediatric Neurology Unit, Tel Aviv Sourasky Medical Center
We thank Dr. Lanska for his comments. There are no confirmed data on the number of children severely affected. The figure of 20 children is the assumed figure. To the best of our knowledge, the seven children reported are the only ones who had severe epilepsy due to thiamine deficiency.
In addition, Dr. Lanska provided history on the issue of thiamine deficiency and epilepsy. [2-4] Our objective was to investigate the development of long- term epilepsy in children who survived severe thiamine deficiency in infancy, a phenomenon that was never previously described in infantile thiamine deficiency. Although we described the seizures that occurred during the acute phase, our aim was to report on the long-term seizures.[1]
We agree with the author that seizures in the acute phase are a known phenomenon in thiamine deficiency in humans and in animal models. This is expected considering the metabolic insufficiency that occurs in thiamine deficiency (i.e., lactic acidosis, hypoglycemia and energy deficiency). However, all the cases described by the author were diagnosed post mortem, suggesting that there was no possibility of residual epilepsy.[2]
Disclosure: The author reports no disclosures.
Epilepsy in children with infantile thiamine deficiency Epilepsy in children with infantile thiamine deficiency
24 November 2009
Douglas J. Lanska, MD, MS, MSPH, FAAN, VA Medical Center 500 E. Veterans St., Tomah, WI 54660
Douglas.Lanska{at}med.va.gov Douglas J. Lanska, MD, MS, MSPH, FAAN
Fattal-Valevski et al. reported on epilepsy in children with thiamine deficiency who had been fed defective soy-based formula as infants.[1]
According to the authors, five or six of the seven children had seizures during the acute period but the frequency of acute seizures among all affected infants was unclear. The relationship between the occurrence of seizures during the acute period and the later development of epilepsy among survivors of clinically significant thiamine deficiency during infancy is also uncertain.
In 1910, McLaughlin and Andrews reported convulsions in 40% of 86 infants found at autopsy to have died due to infantile beriberi. They also found "slight" convulsions in an additional 4 (5%) of these cases.[2] Although this was in an era before the isolation and chemical identification of thiamine, the accuracy of such clinical diagnoses was fairly valid. This validity is based on the high positive predictive value of clinical diagnosis based on autopsy results among those who died; reproduction of the disease in an animal model; and prompt and marked improvement with administration of an extract of rice polishings, which were later shown to have a high concentration of thiamine.[3,4]
As noted by Fattal-Valevski and colleagues, earlier work did not follow survivors longitudinally and did not describe the later development of epilepsy in a large proportion of survivors.
References
1. Fattal-Valevski A, Bloch-Mimouni A, Kivity S, et al. Epilepsy in children with infantile thiamine deficiency. Neurology 2009;73:828-833.
4. Chamberlain WP, Vedder EB. The cure of infantile beriberi by the administration to the infant of an extract of rice polishing, and the bearing thereof on the etiology of beriberi. Bull Manila Med Soc 1912;6:26-33.
Disclosure: Dr. Lanska is on the editorial board of MedLink Neurology; and served as a consultant for Etter, MacMahon, Lamberson, Clary, Troppman & Oreskovich, P.C., Spokane, WA.
