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Recent eLetters

Displaying 1-10 letters out of 492 published

  1. Appropriate baseline setting for the evaluation of treatment

    Troussiere et al. conducted an interesting survey to prevent the progress of Alzheimer's disease in patients with sleep apnoea syndrome (SAS) by continuous positive airway pressure (CPAP) therapy (1). I fundamentally agree with their study outcome. I have a query on the setting of CPAP and non-CPAP groups.

    The cut-off point of 23 for Mini Mental State Examination (MMSE) is widely accepted. The authors mentioned that there was no significant difference in median value MMSE at baseline between two groups, but the max value of MMSE in 9 patients without treatment of CPAP was 24. On this point, I cannot ignore the 3.5 difference of median value. MMSE is one of the screening questionnaires and it reflects the progress of cognitive function in each patients.

    Vos et al. investigated the prevalence and long-term outcome of preclinical Alzheimer's disease according to the following criteria: cognitively normal individuals with abnormal amyloid markers (stage 1), abnormal amyloid and neuronal injury markers (stage 2), or abnormal amyloid and neuronal injury markers and subtle cognitive changes (stage 3), by follow-up 311 participants, aged 65 or older, with clinical dementia rating of 0 (2). The 5-year progression rate to clinical dementia rating at least 0.5 was calculated, according to the baseline stages. As a result, a symptomatic Alzheimer's disease was 2% for participants classed as normal, 11% for stage 1, 26% for stage 2, and 56% for stage 3, respectively.

    I suppose that baseline allocation of patients into CPAP and non-CPAP groups should be paid with caution, especially in MMSE. If not so, the net effect of CPAP treatment on the progress of cognitive function cannot determine. In addition, during the 3-year follow-up period, there is a possibility in the progress of preclinical Alzheimer's disease. I understand that SAS is not only the factor, but baseline setting is important to know the effect of CPAP therapy in patients with SAS for the progress of cognitive function.

    I also recommend the authors to check the MMSE values more frequently during the 3-year follow-up study.

    References

    1 Troussiere AC, Monaca Charley C, Salleron J, et al. Treatment of sleep apnoea syndrome decreases cognitive decline in patients with Alzheimer's disease. J Neurol Neurosurg Psychiatry 2014 May 14. doi: 10.1136/jnnp-2013-307544

    2 Vos SJ, Xiong C, Visser PJ, et al. Preclinical Alzheimer's disease and its outcome: a longitudinal cohort study. Lancet Neurol 2013;12:957- 65.

    Conflict of Interest:

    None declared

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  2. CT-negative, lumbar puncture-positive and CTA-negative patients have a low risk of aneurysms.

    Dear Editor,

    We are grateful to Bakker et al. for their prospective study in this area.[1]

    Two months prior to this, we published on the topic of CT-negative, lumbar puncture-positive and CT-angiography (CTA) negative patients.[2] Such patients had been reported in 98 published cases. No causative aneurysms were found in neither these nor in the 9 cases which we identified.

    Bakker et al report 37 additional patients in the section 'Imaging' on page 3 of their article. These 37 patients had digital subtraction angiography (DSA) within 48 hours and no vascular lesions were found. This brings the number of published cases to 144.

    We recommend double-reporting of the CT angiogram in these apparently normal scans. The risk:benefit ratio of proceeding to DSA in such patients is debatable due to the relatively small number of published cases.

    Arnab K. Rana[a], Helen E. Turner[b] and Kevin A. Deans[b]

    a Aberdeen Biomedical Imaging Centre, University of Aberdeen, Lilian Sutton Building, Foresterhill, Aberdeen, AB25 2ZD, UK

    b Department of Clinical Biochemistry, Aberdeen Royal Infirmary, Foresterhill, Aberdeen, AB25 2ZN, UK

    References:

    [1] Bakker NA, Groen RJM, Foumani M et al. Appreciation of CT- negative, lumbar puncture-positive subarachnoid haemorrhage: risk factors for presence of aneurysms and diagnostic yield of imaging. J Neurol Neurosurg Psychiatry doi:10.1136/jnnp-2013-305955.

    [2] Rana AK, Turner HE and Deans KA. Likelihood of aneurysmal subarachnoid haemorrhage in patients with normal unenhanced CT, CSF xanthochromia on spectrophotometry and negative CT angiography. J R Coll Physicans Edinburgh 2013; 43: 200-6.

    Conflict of Interest:

    None declared

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  3. Screening for post-stroke depression: caution for meta-analysis

    Meader et al. reported screening abilities of several tools for detecting post-stroke depression by meta-analysis procedures (1). Although the Center of Epidemiological Studies-Depression Scale (CESD), the Hamilton Depression Rating Scale (HDRS) and the Patient Health Questionnaire (PHQ)-9 showed acceptable validity for screening of depression, these tools are not acceptable for clinical use for case- finding. In their article, the authors selected 23 cross-sectional studies and one prospective cohort study, and Hierarchical Summary Receiver Operating Curve (HSROC) meta-analyses were conducted to obtain pooled estimates of sensitivity and specificity and HSROC curves with a minimum of three studies to ensure stable estimates were computed. I think that their statistical procedure is fundamentally adequate, but some concerns are existed. First, there are no available diagnostic criteria specifically for post- stroke depression, and the reference standard for the diagnosis of depression was based on Diagnostic and Statistical Manual-Fourth Edition (DSM-IV) or the International Classification of Disease Tenth Edition (ICD -10) criteria. I suppose that ROC analysis without established reference standard for the diagnosis of depression should be handled with caution. Second, the authors included a one-year cohort study by Kang-et al. (2) for their meta-analysis. To keep sample size of pooled data, inclusion of this cohort study is not a mistake. To specify the change of effect, sensitivity analysis by excluding cohort study should also be conducted for their study. Finally, I speculate the existence of ethnic difference and social development on the screening ability for post-stroke depression. Unfortunately, there is no way to adjust these variables in addition to sex and age, which are fundamental confounders on the risk of stroke. Anyway, diagnostic criteria for post-stroke depression should be urgently determined as the reference.

    References 1 Meader N, Moe-Byrne T, Llewellyn A, et al. Screening for poststroke major depression: a meta-analysis of diagnostic validity studies. J Neurol Neurosurg Psychiatry 2014;85:198-206. 2 Kang HJ, Stewart R, Kim JM, et al. Comparative validity of depression assessment scales for screening poststroke depression. J Affect Disord 2013;147:186-91.

    Conflict of Interest:

    None declared

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  4. Response to research paper of Mr. Wessely

    This letter was published in error. The text is no longer available.

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  5. Porphyric neuropathy

    Reply - We thank Prof Shubhakaran for the interest shown in our article and for highlighting that porphyric neuropathy should be among the differential diagnosis in patients presenting the pharyngeal-cervical- brachial weakness. Indeed, porphyric neuropathy does share some clinical features with Guillain-Barre syndrome and in 50% of cases weakness starts in the upper limbs and therefore may mimic pharyngeal-cervical-brachial weakness. Similar to Guillain-Barre syndrome, progression to nadir occurs by 4 weeks, although in some cases development of tetraparesis and respiratory failure can be rapid. Cerebrospinal fluid may also show albuminocytological dissociation. Similar to pharyngeal-cervical-brachial weakness, nerve conduction studies show axonal-type neuropathy. Porphyric neuropathy, however, is rare and patients invariably complain of severe abdominal pain and develop psychiatric symptoms before developing neuropathy. Neuropathy, when is does occur is usually asymmetric with prominent autonomic involvement, which differentiates it from Guillain- Barre syndrome and indeed pharyngeal-cervical-brachial weakness in most cases. Reference: Albers J W, Fink J K. Porphyric neuropathy. Muscle Nerve. 2004; 30, 410-22.

    Conflict of Interest:

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  6. Re:Levodopa equivalent daily dose and the development of impulse control disorder

    Thank you very much for your interest in our paper and your comments. We have used the levodopa equivalent daily dose (LEDD) of dopamine agonist (ADA) as previously published, and must agree with you as the topic probably needs a thorough review. Anyway, it seems that the occurrence of impulse control disorders (ICDs) in patients with Parkinson's disease (PD) and other diseases in treatment with DA is not just dose-dependent. It is clear that the higher the dose the more prevalent ICDs, but lower doses can also precipitate them (Perez-Lloret et al., 2012; Weintraub et al., 2010). We did not find differences regarding LEDD of rotigotine between PD patients with or without ICD. We may regard this phenomenon as a class effect of rotigotine, as far as we know idiosyncratic, which may imply a pathoplastic effect, as it would change the clinical spectra of the disease.

    Conflict of Interest:

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  7. Psychiatric side effects of rotigotine mirror its different dopaminergic receptors affinity

    Dear Sir,

    We have read with interest the study by Garcia-Ruiz et al.,[1] which investigated the prevalence of Impulse Control Disorders (ICD) in 233 patients with Parkinson's disease (PD) by means of QUIP scale. The authors evaluated for the first time the prevalence of ICD in patients treated with the most commonly prescribed dopamine-agonists (DAs), namely transdermal rotigotine and oral ropinirole and pramipexole. They concluded that oral DAs are significantly more associated with ICD than rotigotine. We would like to bring to the authors' and readers' attention, some methodological issues, which can better guide us in the understanding of psychiatric manifestation caused by the different classes of dopaminergic medications. First, the Authors referred to hobbyism and punding as two separate entities, indeed they might fall within the same spectrum of behavioural disorders starting with an increase of goal-directed activity and ending in a loss of control over the activity, thus becoming "non-goal directed"[2]. Second, the Authors considered punding and ICD as the same disorder. Several lines of evidence suggest that - although often coexisting in the same patient - ICD and punding have a different pathophysiology[2]. In fact, punding seems to be mainly associated with the stimulation of dopamine receptors D1 and D2 whereas ICD might be more related to D2 and D3 receptors agonism. Indeed in our critical review of literature, almost all punding patients reported were on medications acting mainly on receptors D1 and D2 (pergolide, apomorphine, cabergoline and levodopa), while ICD were more frequent in patients taking dopamine agonists than levodopa [2]. Therefore, while Garcia-Ruiz et al.'s study goes beyond the limits of all previous studies, which have considered all DAs as a class, it has the limit of not having clustered the psychiatric complications of DAs according to the different pathophysiological mechanisms. Accordingly, the re-evaluation of the raw data depicted by Figure 1 in Garcia-Ruiz et al.'s study shows that patients on rotigotine experienced punding (plus hobbyism) more frequently than ICD (17% vs. 5%) while patients on oral DA reported about the same prevalence for punding and ICD (38% vs. 28% and 31% vs. 38% for ropinirole and pramipexole, respectively). Unfortunately authors did not report which patients had only punding and which had it associated with ICD, nor how many patients were on DA monotherapy and how many were on a combination of DA and levodopa so that no further speculations are allowed. The study by Garcia-Ruiz et al. indirectly supports the well-established view that punding and ICD are different entities. The high concentration of D3 receptors in the ventral part of the striatum and limbic cortex explain the stronger association of oral DAs with ICD.[3] By contrast, the association of punding with the compulsive use of levodopa[4] as well as the pathophysiology of stereotypies in animals models and humans,[2,5] point to a role of striatal D1 and D2 receptors. Indeed, the receptors binding profile of pramipexole and ropinirole mainly involves dopamine receptors D2 and D3 whereas rotigotine has D1 affinity too. We have here underlined how the manner in which ICD and punding are conceptualized would have important clinical implications for both diagnosis and treatment management, therefore future longitudinal studies are encouraged to better clarify the role of different molecules in the pathophysiology of different types of dopaminergic behaviours.

    REFERENCES

    1. Garcia-Ruiz PJ, Martinez Castrillo JC, Alonso-Canovas A, Herranz Barcenas A, Vela L, Sanchez Alonso P, Mata M, Olmedilla Gonzalez N, Mahillo Fernandez I. . Impulse control disorder in patients with Parkinson's disease under dopamine agonist therapy: a multicentre study. J Neurol Neurosurg Psychiatry. 2014 Jan 16

    2. Fasano A, Petrovic I. Insights into pathophysiology of punding reveal possible treatment strategies. Mol Psychiatry. 2010 Jun;15(6):560- 73.

    3. Weintraub D. Dopamine and impulse control disorders in Parkinson's disease. Ann Neurol 2008 Dec;64(Suppl. 2):S93e100.

    4. Evans AH, Katzenschlager R, Paviour D, O'Sullivan JD, Appel S, Lawrence AD, et al. Punding in Parkinson's disease: its relation to the dopamine dysregulation syndrome. Mov Disord 2004;19:397e405.

    5. Fasano A, Evans AH. Is punding a stereotypy? Mov Disord. 2013 Mar;28(3):404-5.

    Conflict of Interest:

    None declared

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  8. PHARYNGEAL-CERVICAL -BRACHIAL VARIENT OF GUILLAIN BARRE SYNDROME

    I read an interesting article on a variant of Guillain Barre syndrome, by Benjamin and Nobunhiro(March 2014 issue). The review was excellent one but it was lacking one important differential diagnosis among the list of what were mentioned by the eminent authors, that is porphyria1. Porphyric neuropathy is a source of confusion in practice, and patients with porphyria rarely receive the correct diagnosis early in the course of the illness. Porphyric neuropathy is manifest by symptoms, signs, and cerebrospinal fluid resembling acute Guillain- Barre syndrome1. Accompanying psychological features, a proximal predilection of asymmetric weakness, andelectrodiagnostic indicative of an axonal polyradiculopathy or neuropath all suggest the diagnosis of porphyria1. REFRENCES- 1. Albers J W, Fink J K. Porphyric neuropathy. Muscle Nerve. 2004; 30(4): 410-22.

    Conflict of Interest:

    None declared

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  9. Does the link between vitamin D and depression have a role in future multiple sclerosis research?

    Dear Authors,

    Thank you for this fascinating paper. Despite the study finding no causal association between the risk of multiple sclerosis (MS) and major stressful life events, the premise lends itself to consider the association between MS and other stress-related factors.

    The increasingly important relationship between a lack of vitamin D and a higher incidence of MS has been researched in depth (1). Despite a lack of association between major stressful events and the risk of MS, stress is known to induce symptoms of depression. Studies have shown how levels of vitamin D are inversely proportional to the presence of depressive symptoms in MS patients (2). However, the link between vitamin D, risk of MS and depression (pre-diagnosis) has yet to be researched. Depression is now known to be associated with low-grade inflammatory responses (3). One way in which vitamin D affects our immune system is by inducing a switch from the production of inflammatory cytokines to anti- inflammatory cytokines (an example being IL-10) (4).

    As a vitamin D deficiency is easily correct and the link between vitamin D and both depression/MS is becoming increasingly clear, it would be interesting to note the relationship between clinical depression and the risk of MS. This may become an important area of research in light of the rising number of MS sufferers.

    1. Summerday, N., Brown, S., Allington, D., Rivey, M. Vitamin D and Multiple Sclerosis Review of a Possible Association. Journal of pharmacy practice. 2012; 25 (1): 75-84.

    2. Ashtari, F., Ajalli, M., Shaygannejad, V., Akbari, M. and Hovsepian, S., 2013. The relation between Vitamin D status with fatigue and depressive symptoms of multiple sclerosis. Journal of research in medical sciences: the official journal of Isfahan University of Medical Sciences, 18(3), p.193.

    3. Berk M, Williams LJ, Jacka FN, O'Neil A, Pasco JA, Moylan S, et al. So depression is an inflammatory disease, but where does the inflammation come from? BMC Med. 2013;11 200.

    4. Ho S, Alappat L, Awad A. Vitamin D and Multiple Sclerosis. Critical Reviews in Food Science and Nutrition. 2012; 52(11).

    Conflict of Interest:

    None declared

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  10. Levodopa equivalent daily dose and the development of impulse control disorder

    We have read your paper regarding impulse control disorders (ICDs) in Parkinson's patients receiving dopamine agonist therapy with great interest. Although the stability in plasmatic levels or the route of administration of the agonist may play a role in the development of ICDs just as they might explain the occurrence of motor dyskinesias, a dose- response curve would also be expected. While the levodopa equivalent daily dose (LEDD) of rotigotine has not been delimited between those with and without ICDs, the average LEDD in the group is higher than that of patients receiving oral agonists, yet with a lower incidence of ICDs. This calls for a further review of the published equivalencies for antiparkinsonian drugs, especially those with less studies supporting the available conversion formulae.

    Conflict of Interest:

    None declared

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