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Recent eLetters

Displaying 1-10 letters out of 72 published

  1. CSF Evaluation

    Is there any reason you can think of when the CSF protein and the CSF glucose should be evaluated from different tubes of CSF and not the same tube?

    Conflict of Interest:

    None declared

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  2. How I start a new patient consultation-view from across the pond

    I read with interest Allen et al. approach to starting a new patient consultation1. Apart from a few minor differences the basic methodology employed by all four physicians is essentially the same. Across the pond, I start a new patient consultation in much the same way. I walk into the reception area, call out the patient's name and upon acknowledgement ("right here" or "yes" is the usual response, rarely "yo" and I have still to hear someone say "present); I introduce myself to the patient and then proceed to walk the patient and the accompanying caregiver or friend to the examination room assigned to me for that day. During the short walk I may exchange a few brief pleasantries, the weather or the traffic always are safe bets to elicit an answer from even the most stoic of patients! ("It sure is hot today" or "did you have a tough time driving into the city today?"). This helps to break the ice and my next question after everyone is seated comfortably in the room is "So Ms Watson what brings you in to see my today?" I then allow the patient or the caregiver (both at times) to speak uninterrupted for the next few minutes as I record their words verbatim on a piece of paper. I make it a point to look up at the patient from time to time to acknowledge that he or she has my rapt attention. This is contrary to some of my colleagues who prefer to type the history into the electronic health record (EHR) at the same time. I feel this makes the encounter rather aseptic (with the physician typing vigorously into the computer at times with his back to the patient) and so I prefer to type my notes into the EHR either immediately after the conclusion of the patient encounter or at the end of the day. I then ask a few direct questions frequently to clarify some aspects of the patient's history and then move on to the relevant past medical history, list of current medications, social and family history and finally a brief review of the systems. Then follows the neurological examination and it is not infrequent that I may ask a few direct questions at this stage too ("does it hurt here" "where does the pain radiate?"). I devote the last 10-15 minutes of a new patient consultation (a new patient consultation is typically an hour in duration) to explain my assessment and plan and answer any questions. I end the encounter by walking the patient over to my secretary so that she can help schedule the tests ordered and a follow up consultation if warranted.

    References

    1. Allen C, Scolding N, Mumford C, Smith P, Fuller G. How I start a new patient consultation. Pract Neurol 2013; 13:254-7.

    Conflict of Interest:

    None declared

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  3. HIV testing in a patient presenting with cognitive impairment-to test or not to test

    I read with interest the debate between Nightingale el al. and Schott about whether we should routinely test for HIV in patients presenting with cognitive impairment 1,2 . I assume that while the authors have taken rather polarized views to state their point, the correct answer lies somewhere in between. Testing for HIV shall not be the foremost in my mind in a 75-year-old male presenting with slowly progressive cognitive impairment for the past few years accompanied with typical features of a cortical dementia (aphasia, apraxias and agnosias). In such a patient I shall rather harness my clinical and diagnostic skills to differentiate between Alzheimer's disease, frontotemporal dementia and Lewy body dementia. On the other hand a 45-year-old male presenting with cognitive impairment accompanied by a movement disorder, certainly HIV testing shall be included in my diagnostic armamentarium. One must though not forget that positive HIV serology is not synonymous with HIV encephalopathy or AIDS dementia complex which is a clinical syndrome comprising of a combination of cognitive, behavioral and motor dysfunction. Testing a patient with cognitive impairment for HIV shall have a high positive predictive value only when the test is carried out after taking the patient's age at presentation, history (not just of risk factors but also of the rate of progression of symptoms) and examination findings into consideration.

    References

    1. Nightingale S, Michael BD, Defres S, Benjamin LA, Solomon T. Test them all; an easily diagnosed and readily treatable cause of dementia with life-threatening consequences if missed. Pract Neurol. 2013;13:354-6.

    2. Schott JM. HIV testing in dementia: test some, perhaps more, but not all. Pract Neurol. 2013;13:357-8.

    Conflict of Interest:

    None declared

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  4. aetiology of myoclonus

    sir/madam,

    Can myoclonus involve large muscles like the trunk muscles giving out just one jerk with a duration of a fraction of a second?Would it be justified to term this phenomena as a myoclonic seizure or a complex myoclonus when there is LOC for that fraction of a second;happening while falling asleep only.Or can it be a sleep disorder,a hypnic jerk?

    Conflict of Interest:

    without reading the entire text how can I declare any competing interests.

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  5. Pre-protocol experience from Belfast.

    We welcome the article by Jones et al, and in particular the chance to compare the protocol used in their institution with the one we hope to implement (1).

    In Northern Ireland, we are in the process of drawing up a regional protocol for the management of status epilepticus, due to wide variation in current practice. We carried out preliminary work to see where the gaps in knowledge are, so that we can create a relevant protocol to assist junior staff, hopefully highlighting the need for a protocol.

    We surveyed post finals - final year medical students (9 students) foundation (28 doctors) and core medical trainees (24 doctors) and got 61 responses to a questionnaire (~85% returns). Only 10% of these knew the appropriate dose and rate of administration of two first line drugs.

    Only 54% would have given an initial 4 mg dose of lorazepam, and only 36% knew the correct dose of phenytoin (15-20mg/kg); 44% acknowledged they were unaware of the dose. One third knew the appropriate initial infusion rate of phenytoin.

    Knowledge of the side effects of phenytoin was generally good, although worryingly 30% thought sedation was a side effect of phenytoin, which might lead to complacency in managing the apparently "post ictal" patient.

    It was also evident that a significant issue for junior doctors is making the actual diagnosis of status epilepticus. Without clinical experience junior doctors lack ability in making a confident and accurate diagnosis, for which they are prepared to give drugs which are sedating and are perceived to be potentially dangerous. In addition doctors in the early stages of training had limited appreciation of potentially discriminant features such as back arching, biting the tip of the tongue, open eyes during the event and the synchrony of limb movements, in making a clinical diagnosis of seizure versus non epileptic attack disorder.

    Better educational strategies that inform, everyone who manages status epilepticus, about seizure semiology (2) would go hand in hand with dissemination of treatment protocols and would therefore be useful.

    We wish to add another vitally important point to the protocol by Jones et al, and that is the clear instruction to seek immediate urgent advice from the nearest neurology service in all cases of status epilepticus.

    (1) Jones S, Pahl C, Trinka E, et al. A protocol for the inhospital emergency drug management of convulsive status epilepticus in adults. Practical neurology 2014;14:194-197

    (2) Seneviratne U, Ding C, Bower S et al. Video based training improves the accuracy of seizure diagnosis. J Neurol Neurosurg Psychiatry 2014;85:466-470

    Conflict of Interest:

    None declared

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  6. Re:What is the risk of PCP in patients with neurological disease?

    We thank Dr Lilleker for his comments. We agree that use of PCP prophylaxis must provide benefit that would outweigh any attendant risk. As suggested in our article, this risk is likely to vary depending on the dose and duration of steroid therapy, the co-administration of other biologicals and the systemic health of the patient. A patient with e.g., systemic vasculitis-associated mononeuritis multiplex who has also been treated with cyclophosphamide is likely to be at much higher risk than in the cited example of an individual with myasthenia. The potential toxicity of trimethoprim-sulfamethoxazole may be augmented through use of a lower 80/400mg daily dose; or through use of alternate day 160mg/800mg dosing. Recent data from the field of rheumatology suggests that the overall risks of prophylaxis are low and the prophylactic benefit high [1]. Ultimately, we agree with the correspondent that knowledge of the incidence for PCP in our immunosuppressed patients would best guide application of such data in clinical practice. Since publication, others have shared empiric experience of adverse outcomes in those not placed on prophylaxis. Awaiting definitive data, the decision remains with the individual clinician; taking into account the risk factor profile mentioned above.

    Reference [1] Katsuyama T, Saito K, Kubo S, Nawata M, Tanaka Y. The prophylaxis for Pneumocystis pneumonia in patients with rheumatoid arthritis treated with biologics, based on risk factors found in a retrospective study. Arthritis Res Ther. 2014 Feb 5;16(1):R43. PubMed PMID: 24495443; PubMed Central PMCID: PMC3978920.

    Conflict of Interest:

    None declared

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  7. What is the risk of PCP in patients with neurological disease?

    I thank the authors for highlighting this difficult topic with a very thought provoking article.

    In immunosuppressing a patient with neurological disease, as with anything a physician does to a patient, there are potential risks to take into account and to be weighed up against the proposed benefits. Indeed, this sort of "cost-benefit" analysis is a central tenant of decision making in much of life outside of medicine also.

    It is generally accepted that in order to proceed, the benefits should outweigh the "costs". It is clear that PCP prophylaxis is effective at reducing the incidence of PCP, but at what cost? In patients with solid -organ transplant for example, this is fairly clear as the incidence appears high, as noted in the authors references.

    The problem is that we have little knowledge of the incidence of PCP in patients immunosuppressed for myasthenia gravis, for example. My personal feeling is that this risk is much lower, but there is little evidence in the literature to support this.

    When considering that around 15% of patients develop side effects whilst taking trimethoprim-sulfamethoxazole, and these can (in rare cases) be fatal, it is not clear in my mind that the cost-benefit analysis for patients with neurological disease swings in favour of the widespread use of PCP prophylaxis. Put simply, would enough cases of PCP be prevented to outweigh the risks posed by the side effect profile of the medication?

    To help us make this decision we need clearer data on the incidence of PCP in patients with neurological diseases who are being prescribed immunosuppressive medication.

    Conflict of Interest:

    None declared

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  8. 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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  9. 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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  10. 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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