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Recent eLetters

Displaying 1-10 letters out of 65 published

  1. Superb Book

    This is a superb book that deserves to be better known, at least on my side of the Atlantic. In addition to Barker's outstanding depiction of WW1 Britain, the sympathetic and revealing exploration of the physician- patient relationship is peerless. Interested readers should know that Regeneration is the first book in a trilogy, though neither is quite as good as Regeneration. The second book, The Eye in the Door, is quite good. The final book, The Ghost Road, is a bit uneven but the final section of this book, describing an infantry assault in the closing stages of the war, is an absolute tour-de-force of sympathetic description.

    Conflict of Interest:

    None declared

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  2. Chocolate Consumption, Nobel Prizes and -Scientific Integrity

    In a paper published last year in the New England Journal of Medicine (NEJM), Messerli noted "a surprisingly powerful correlation between chocolate intake per capita and the number of Nobel laureates in various countries," which he postulated as "most likely" related to the cognitive enhancing benefits of chocolate.1 This article in one of the premier journals in the world received extraordinary press reports around the time of its release including in television (BBC News, CBC) and print (Time, Reuters, Associated Press, and Forbes) media. We found substantial methodological and conceptual errors in the Messerli article that we brought to the attention of the editor of the NEJM shortly after its publication. However, much to our surprise and dismay, no letter to the editor (including ours), note or article addressing these concerns have appeared in the NEJM since publication of the original article, although several authors have subsequently brought several statistical criticisms to light in other journals,2-5 including Practical Neurology. While several authors who have criticized the Messerli article have done a wonderful job of highlighting the limitations of association studies, no one, to date, has addressed two issues we feel are even more important to the scientific process: 1. Messerli's use of secondary sources (i.e., Wikipedia) for his data and 2. Messerli's selective use of data to support his hypothesis. In his article, Messerli notes, correlation does not "prove" causation and he notes he lacks the specific chocolate intake of individual Nobel Laureates. However, correlation between 2 variables is frequently used for hypothesis generation and Messerli suggests several hypotheses to account for his correlation. First, hypotheses generated from data are, of course, no better than the data on which they are based. Therefore, it is essential that authors use primary sources when possible. Messerli used data on Nobel laureates from Wikipedia6, which were based upon a BBC source, instead of data obtained directly from the Nobel Prize website7 which is readily available. The distinction is important and changes the resultant number of awardees based upon whether one chooses to count a Nobel laureate who is born in a country or where the person is located at the time of the award. For example, there are 323 Nobel laureates (1901-2012) who were affiliated with an organization in the USA at the time they were awarded the Nobel prize and 247 Nobel laureates who were born in the USA.7 Second, and perhaps even more important than the sources from which data are drawn, is the use of complete data sets and not just those that support a hypothesis. The selective use of data from secondary sources has no place in science to support, refute or generate hypotheses. This is a serious methodological lapse and is called into question by the following: 1. Wikipedia lists 71 countries with per capita Nobel laureate data6, yet only 23 were selected for Messerli's analysis; and 2. Data on chocolate consumption used were from non-contiguous years (2002, 2004, 2010 and 2011) although data from the same sources are available for multiple intervening years and per capita chocolate consumption for countries also change from year to year but Messerli chose certain data while excluding other data. Which data were selected skews the correlation substantially. For example, if one selects the top 10 chocolate consuming countries and using Messerli's data, the correlation is non-existent (r2= 0.04). It is important to remember in any hypothesis generating study that bias is easily introduced into that study through design flaws (e.g., selective use of data or use of secondary sources) as well as known statistical artifacts (e.g., ecological analysis2). Such bias can render the study completely useless or, worse, damages the integrity of the scientific process and the peer-review process of publication. As with others in the medical and scientific community2-5 and the press, we did not see Messerli's article as a joke intended by the author and the NEJM. However, we assert that if an article is published in a medical journal draws widespread publicity and is interpreted inappropriately as a valid scientific study, it is the responsibility of the editors of that journal to clarify the misinterpretation. Otherwise, the integrity of all scientific journals may become suspect. This will be the subject of an editorial in Practical Neurology. Competing Interests: None Contributorship statement: This article was originally conceived by BDP and was discussed with the other two authors who helped in the analysis and writing of the original article and its reviews. Each author contributed to the writing and revision of this revised article and approved the final version.

    References 1. Dunstan, F. Nobel Prizes, Chocolate and Milk: The Statistical View Pract Neurol 2013;13:206-207. 2. Messerli, F.H. Chocolate Consumption, Cognitive Function, and Nobel Laureates N Engl J Med 2012;367:16:1562-4. 3. Maurage, P., Heeren, A., Pesenti, M. Does Chocolate Consumption Really Boost Nobel Award Chances The Peril of Over-Interpreting Correlations in Health Studies" J Nutr 2013;143:931-933. 4. Kayser, M. Editor's pick: Christmas is coming-time for chocolate to get ready for your Nobel Prize Investigative Genetics 2012;3:26. 5. Linthwaite, S., Fuller, G.N., Milk, chocolate and Nobel prizes Pract Neurol 2013;13:63. 6. List of countries by Nobel laureates per capita [Internet]. San Francisco: Wikipedia.-[accessed 2012 October 25]. Available from: http://en.wikipedia.org/wiki/List_of_countries_by_Nobel_laureates_per_capita 7. The Official Website of the Nobel Prize [Internet]. [accessed 2013 May 30]. Available from www.nobelprize.org.

    Conflict of Interest:

    None declared

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  3. Spontaneously resolving cerebellar syndrome as a sequelae of dengue viral infection

    Sir, the report on "spontaneously resolving cerebellar syndrome as a sequelae of dengue viral infection" is very interesting [1]. In fact, neurological complication of dengue is not common but it can be detectable [2]. The spontaneously resolving cerebellar syndrome in this report is questionable for the relationship to dengue. Based on the previous study from Thailand, the spontaneously resolving pathology of cerebellum was not detected [3]. Although virus can be detected at cerebellum it is usually identified in death cases [3 - 4].. The case of spontaneously resolving cerebellar syndrome is usually identified in the patients with concurrent infection between dengue and Epstein-Barr virus infection [5]. The interesting topic is whether there is any interaction during co-infection that contribute to observed cerebellar pathology.

    References 1. Weeratunga PN, Caldera HP, Gooneratne IK, Gamage R, Perera WS, Ranasinghe GV, Niraj M. Spontaneously resolving cerebellar syndrome as a sequelae of dengue viral infection: a case series from Sri Lanka. Pract Neurol. 2013 Jul 9. [Epub ahead of print] 2. Wiwanitkit V. Dengue fever: diagnosis and treatment. Expert Rev Anti Infect Ther. 2010 Jul;8(7):841-5. 3. Wiwanitkit V. Magnitude and pattern of neurological pathology in fatal dengue hemorrhagic fever: a summary of Thai cases. Neuropathology. 2005 Dec;25(4):398. 4. Ramos C, S?nchez G, Pando RH, Baquera J, Hern?ndez D, Mota J, Ramos J, Flores A, Llaus?s E. Dengue virus in the brain of a fatal case of hemorrhagic dengue fever. J Neurovirol. 1998 Aug;4(4):465-8. 5. Karunarathne S, Udayakumara Y, Fernando H. Epstein-Barr virus co- infection in a patient with dengue fever presenting with post-infectious cerebellitis: a case report. J Med Case Rep. 2012 Jan 30;6(1):43.

    Conflict of Interest:

    None declared

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  4. Neurophilia! Not.

    I really enjoyed Dr. Fuller's wonderful article on a likely emerging public and professional fascination with neurology. The bad news, however, is humankind's perpetual fascination with phobias; a fascination with 'death' being but one example. I'd perhaps say that neurology has joined some rather elite company.

    I would postulate that neurophobia, rather than neurophilia, drives the impetus to produce copious articles and books on neurology. I am still hopeful that all the books I have purchased on neurology will miraculously cure me of my phobia (notwithstanding the fact that reading neurology texts convinces me that I have alexia).

    Medscape's 2012 Physician Lifestyle Report by Dr. Carol Peckam has neurologists tied for first place as the most unhappy of campers. So, no cigar there either.

    I applaud Dr. Fuller again for the propaganda piece on neurology: I hope it works.

    Conflict of Interest:

    None declared

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  5. The use of stimulation single fibre EMG in investigation of congenital myasthenia

    We enjoyed the review by our colleagues Finlayson et al 1 from the United Kingdom, Congenital Myasthenic service, covering all aspects of the congenital myasthenic syndromes. We would, however, suggest that the section on neurophysiology could have been expanded and elaborated more. To state that the neurophysiological findings in congenital myasthenic syndromes are similar to those in autoimmune myasthenia gravis is correct perhaps with respect to repetitive nerve stimulation but when talking about single fibre EMG (SFEMG) it should be emphasised for accuracy that it is stimulated single fibre EMG (StimSFEMG) that should be used in children, certainly under the age of eight years or in the intensive care setting, and not the voluntary SFEMG technique, which requires significant levels of patient cooperation. Furthermore, with most congenital myasthenic syndromes (CMS) having symptoms at birth, which do not always include ptosis, the use of StimSFEMG should be encouraged as it has superior sensitivity in comparison to repetitive nerve stimulation, which makes it the better screening test. The test is well tolerated and is usually performed in the outpatient setting with the child awake. The problem of the specificity of StimSFEMG can be addressed if the technique is used as part of a more wide-ranging neurophysiological examination including nerve conduction studies and EMG examination of limb and bulbar muscles. As an example, demonstration of significant myopathic changes in other muscles will direct the clinician more to the diagnosis of a myopathy with associated secondary neuromuscular transmission defect rather than a primary myasthenic syndrome. We do not hesitate to use Stim SFEMG, which is well tolerated even by the youngest of infants, and consequently we have seen a decrease in both the age at referral for investigation and subsequent diagnosis over the years. This approach has to be encouraged as in several studies it is clear that in many children with CMS, symptoms have been present from birth, which are often non-specific, such as feeding difficulties 2 or stridor 3. Many of us have experienced the consequences of delayed diagnosis, regrettably including sibling death, and we feel that the liberal use of this excellent technique has been a major factor in preventing this by providing an early diagnosis. In an article for a wide readership it is perhaps an omission not to use this opportunity to advertise this technique, available at many Neurophysiological centres (including those of the authors). Hopefully this letter will in part address this oversight.

    Reference List

    1 Finlayson S, Beeson D, Palace J. Congenital myasthenic syndromes: an update. Pract Neurol 2013;13:80-91.

    2 Kinali M, Beeson D, Pitt MC, et al. Congenital Myasthenic Syndromes in childhood: Diagnostic and management challenges 1. J Neuroimmunol 2008 15;201-202:6-12.

    3 Jephson CG, Mills NA, Pitt MC, et al. Congenital stridor with feeding difficulty as a presenting symptom of Dok7 congenital myasthenic syndrome. Int J Pediatr Otorhinolaryngol 2010;74:991-994.

    Conflict of Interest:

    None declared

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  6. Functional symptoms in neurology-making the right diagnosis

    The borderland between functional diseases and neurological diseases gets blurred especially when the patient presents with a myriad of symptoms which do not localize to any one level of the neural axis.1 If in addition the neurological examination is normal (especially the lack of 'hard' neurological signs such as upgoing plantars, cranial nerve signs, definite asymmetry of the deep tendon reflexes, cerebellar signs and gait disorder) the question of a functional disease certainly crosses the mind. In my mind there are two ways to approach such patients. One way is to order an exhaustive battery of tests including laboratory, neurophysiology and neuroimaging studies. This "fishing" for an answer approach rarely if ever yields the answer and risks reinforcing the sick role in the patient's and caregiver's psyche ("I must have a horrible and terrible illness which the doctor is trying hard to find"). The other approach is one I have adopted in my practice. If after a thorough history, examination and relevant investigations the answer still eludes me and I am reasonably certain (though not 100% sure) that the patient's presentation is unlikely on account of an organic neurological disease, I adopt a policy of wait and watch after reassuring the patient that if new symptoms were to appear or if the current symptoms were to change in frequency or intensity, I would consider re approaching the diagnosis. The patient at this point may or may not be ready to see a psychiatrist but I do suggest that consulting one may be helpful.

    References

    1. Stone J, Reuber M, Carson A. Functional symptoms in neurology: mimics and chameleons. Pract Neurol 2013; 13:104-13.

    Conflict of Interest:

    None declared

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  7. Shying away from making a clinical diagnosis

    Turner and Talbot rightly emphasize that in spite of advances in EMG techniques and emergence of novel neuroimaging and CSF biomarkers the diagnosis of motor neuron disease (MND) still remains a clinical one.1 Find upper motor neuron (UMN) and lower motor neuron (LMN) signs in the same limb and MND should be high up in the differential I recall was taught to me in medical school. EMG was to be used in atypical cases where the diagnosis was in doubt. In today's world the pendulum has swung to the other extreme. UMN and LMN signs in the same limb-->could be MND--- >order a 4 limb EMG making certain that tongue and paraspinal musculature is examined-->then make the call-->definite MND Vs probable Vs possible. This over reliance on neuroimaging and neurophysiological data to make the diagnosis is not unique to MND; multiple sclerosis (MS) is another causality. Two discreet attacks separated by time (determined by history) and space (determined by examination findings) and the diagnosis of MS can be made confidently. No MRI brain, visual evoked potentials, somatosensory evoked potentials or oligoclonal bands in CSF are needed. How many of us do that now?

    References

    1. Turner MR, Talbot K. Motor neurone disease is a clinical diagnosis. Pract Neurol. 2012 Dec; 12(6):396-7.

    Conflict of Interest:

    None declared

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  8. Help!-I have a bad case of neurophilia

    Neurophilia can be loosely defined as the love of or fascination for neurology. Now you may think this is a new recently described exotic neurological syndrome but dwell into the ancient eastern Hindu and Buddhist philosophies and you shall quickly realize that the disorder is as ancient as these civilizations themselves 1. The workings of the brain and of the mind fascinated these first neurophilia inflicted philosophers and they spent an inordinate amount of time trying to decipher its secrets. Techniques to control the mind through meditation and introspection were described and perfected over the years. One can imagine these neurophiles wondering how this roughly 1400 gram lump of wrinkled tissue with no moving parts, no joints or valves could function as the motherboard for all other body systems as well as serve as the seat of the mind, thoughts, senses; in fact the very essence of the individual. As we slowly unlock the secrets of the living brain with the aid of sophisticated imaging techniques, the prevalence of neurophilia has increased exponentially. One would not be wrong to label it currently as a pandemic. Identification of this disorder is relatively easy.

    Five signs that you may have neurophilia (in no particular order of importance) 1. You cannot wait for the next book by Oliver Sacks or V.S Ramachandran to come out. 2. You think Dr. House should only concentrate on neurology cases henceforth (a variation of this sign was first described by Dr. Fuller) 3. You name your first and only child "Brain" 4. You identify a Queen Square reflex hammer , a tuning fork and a Wattenberg pin among your priciest possessions 5. You count diagnosing passers-by with Parkinson's disease by mere observation of their gait as one of your favorite pastimes.

    Once inflicted with neurophilia the "disease" course is highly variable. In some it merely manifests with a curiosity to know more about the workings of the brain, yet in others (like us neurologists, neurosurgeons and neuroscientists) it becomes a lifelong obsession to know everything about the brain both in disease as well as in health. My own passion for neurology was kindled at a young age by my neurophilia inflicted neurologist father. Little did I realize that exposure at a tender age would result in such a passion for the study of the brain. Yes it is true and I admit it proudly-I have a bad case of neurophilia. Watch out people it is contagious!

    References 1. Fuller GN. Neurophilia: a fascination for neurology--a new syndrome. Pract Neurol. 2012; 12:276-8.

    Conflict of Interest:

    None declared

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  9. Familial Neurophilia - Is neurophilia hereditary?

    I enjoyed Fuller's description of 'neurophilia' - we can finally label this condition afflicting neurologists, and recognise that is widespread within medicine and the general population.(1) Neurophilia is probably infectious (i.e. environmental); my personal experience and informal discussions with neurology colleagues revealed that many chose neurology as a career following positive experiences during their Senior House Officer jobs. This emphasizes the suggestion that neurophobia can be dispelled and neurophilia encouraged through effective, inspirational teaching, accessible textbooks and journals.

    However, I would also like to highlight a potential genetic contribution. In the UK, I am aware of at least 6 neurological families - those families where more than one first degree relatives are neurologists. - many more than would be expected by chance. This does suggest that neurophilia may have genetic as well as environmental elements.

    Reference 1. Fuller GN. Neurophilia: a fascination for neurology--a new syndrome. Practical Neurology. 2012;12(5):276-8.

    Conflict of Interest:

    Dr Wong is a committed neurophile

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  10. SUDEP-useful information or TMI?

    I read with interest the article by Dr. Leach. As things stand at present, it is not mandatory for physicians in the United States to discuss about SUDEP with patients or their caregivers. In fact this was not included in the recently released American Academy of Neurology (AAN) performance measures for epilepsy 1. Advice about safe recreation and driving though is included as one of the 8 performance measures. So is information about SUDEP useful or too much information (TMI)? Does every patient with epilepsy warrant this information? What is the ideal time to impart this information to the patient and the caregivers: first office visit where this information competes with other "more relevant" information about anticonvulsant dosing, side-effects and importance of compliance for the patient's attention or in subsequent office visits when the patient's seizure semiology and frequency is better characterized? No two patient's seizure disorder is exactly alike hence the potential risk of SUDEP varies from patient to patient. So it reasons that information about SUDEP needs to be customized to the individual patient at hand. Both Dr. Leach's article and my letter raise more questions than answers. In the meantime we are all left pondering how to impart this information to our epilepsy patients and importantly how to do that and take a detailed history, fulfill the performance measures for epilepsy, exam the patient and document this all in the 1 hour allocated for a new patient visit.

    Reference

    1. Fountain NB, Van Ness PC, Swain-Eng R, Tonn S, Bever CT Jr; American Academy of Neurology Epilepsy Measure Development Panel and the American Medical Association-Convened Physician Consortium for Performance Improvement Independent Measure Development Process. Quality improvement in neurology: AAN epilepsy quality measures: Report of the Quality Measurement and Reporting Subcommittee of the American Academy of Neurology. Neurology. 2011 Jan 4;76(1):94-9

    Conflict of Interest:

    None declared

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