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Recent eLetters

Displaying 1-10 letters out of 75 published

  1. Undiagnosing neurological disease

    With great interest I read Coebergh et al. piece on how to undiagnose neurological disease. 1 My experience as a neurologist with subspecialty training in epilepsy has taught me that diagnostic labels such as seizure disorder or epilepsy once attached are very hard to purge either from the patient's medical records or his memory. I frequently encounter patients carrying a diagnostic label of epilepsy in whom continuous video-EEG monitoring reveals non-epileptic events. The record shows no interictal epileptiform features and I feel reasonably confident in undiagnosing their seizure disorder. Taking away their diagnosis of epilepsy is though easier said than done as frequently an abnormal EEG has been reported in the past. Maybe the patient suffers from epileptic as well as non- epileptic events. Maybe I should continue the anticonvulsant to be on the safe side. My patient too is apprehensive and not keen on shedding his diagnostic label. Status quo is maintained.

    References

    1. Coebergh JA, Wren DR, Mumford CJ. Undiagnosing' neurological disease: how to do it, and when not to. Pract Neurol 2014;14:436-439.

    Conflict of Interest:

    None declared

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  2. Re:The article by Zanette et al (2014;14:351-353). T

    We thank Dr. Davenport for his interest in our case report [1] and the opportunity to better explain our clinical reasoning. In his e-letter Dr. Davenport argues that there is a discrepancy between the distribution of the pain, which appeared more suggestive of L2 and perhaps a contribution of L1 and L3, and the involvement of L4 root as documented by clinical neurophysiology and neuroimaging. The patient was asked to draw the distribution of pain on a body diagram with no suggestion from any of us,[2] and some degree of inaccuracy in drawing pain distribution cannot be completely ruled out. However, the most likely explanation for the discrepancy between the reported pain distribution and the anatomical dermatome charts is the presence of referred pain and central sensitization, two phenomena that are known to contribute to the presence of non-anatomical and/or enlarged distribution of neuropathic pain.[3] A pain duration longer than 2 years, as in our case, strongly supports the view of central sensitization. The second point raised by Dr. Davenport concerns the notion that a depressed knee jerk mainly suggests L3 instead of L4 damage. The knee jerk is mediated by the L3 and L4 roots, and its depression, as in the present case, might be secondary to L4 radiculopathy.[4]

    With best regards, Giampietro Zanette MD, Francesca Magrinelli MD, Stefano Tamburin MD

    References 1. Zanette G, Magrinelli F, Tamburin S. Periodic thigh pain from radicular endometriosis. Pract Neurol 2014;14:351-3. 2. Magrinelli F, Zanette G, Tamburin S. Neuropathic pain: diagnosis and treatment. Pract Neurol 2013;13:292-307. 3. Zanette G, Cacciatori C, Tamburin S. Central sensitization in carpal tunnel syndrome with extraterritorial spread of sensory symptoms. Pain 2010;148:227-36. 4. Mumenthaler M. Neurologic Differential Diagnosis; translated and annotated by Otto Appenzeller, 2nd ed. New York, NY: Thieme Publishing Group. 1992:26-27.

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    None declared

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  3. The article by Zanette et al (2014;14:351-353). T

    I thoroughly enjoyed the article by Zanette et al (2014;14:351-353). The authors are to be congratulated for their skilful history taking skills, specifically the key observation that the pain coincided with menses, suggesting the diagnosis, and thus confirming that a neurology opinion, far from being "the last resort", should have been the "first resort". I am troubled by the distribution of the pain however; the authors' thesis, elegantly supported by the neurophysiology and exquisite imaging, is that the pain was due to endometriosis affecting the left L4 root. However, the distribution of the pain appears more suggestive of mainly L2, and perhaps a contribution from L1 and L3 - they also mentioned a depressed knee jerk, which is mainly L3. Most of us regard the L4 dermatome as being below the knee and medial. Whilst I do not dispute the diagnosis of endometriosis, I am intrigued by this, and wonder how the authors explain the dermatomal discrepancy?

    With kind regards Richard J Davenport DM FRCP Edin Consultant Neurologist rjd@skull.dcn.ed.ac.uk Voicemail: 0131 537 3590 NHS PRACTICE Department of Clinical Neurosciences Western General Hospital Edinburgh EH4 2XU Secretary telephone: 0131 537 2072 Fax: 0131 537 1132 Royal Infirmary of Edinburgh MOPD 2 51 Little France Crescent Old Dalkeith Road Edinburgh EH16 4SA Secretary telephone: 0131 242 1487 PRIVATE PRACTICE Spire Murrayfield Hospital 122 Costorphine Road EDINBURGH EH12 6UD Telephone: 0131 334 0363 Spire Shawfair Park Hospital 10 Easter Shawfair Edinburgh EH22 1FE Telephone: 0131 654 5600

    Conflict of Interest:

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  4. 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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  5. 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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  6. 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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  7. 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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  8. 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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  9. 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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  10. 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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