Neurol Ther (2018) 7:165–167 https://doi.org/10.1007/s40120-018-0099-7 LETTER Author’s Response to the Letter to the Editor Regarding: Practical Treatment of Lewy Body Disease in the Clinic: Patient and Physician Perspectives Elisabet Londos Received: February 20, 2018 / Published online: April 27, 2018 The Author(s) 2018 Brzezicki and Kobetic’s  comments on the probably because his main complaint was for- case of a patient with Lewy Body Dementia  getfulness. However, the patient also described are important. Diagnostic precision and con- difﬁculties with mathematics (he had previ- sideration of possible differential diagnoses ously been very good at this) and episodic should, of course, be the foundation of suc- confusion. The CSF investigation showed a total cessful treatment. tau of 510 ng/ml (\ 400), beta-amyloid 340 ng/ In dementia with Lewy bodies (DLB), we are ml ([ 550), P-tau 72 ng/ml (\ 80) and neuroﬁl- bound to rely on the clinical criteria  after ament (NFL) 1120 ng/ml (\ 1850) (with refer- having determined whether the state is a neu- ence values in parentheses) interpreted as a rocognitive disorder of minor or major type slightly increased T-tau and decreased beta- according to diagnostic and statistical manual amyloid level. However, the P-tau level was not of mental disorders (DSM5) . In the actual increased, which would have been a stronger patient’s case, he could not and still cannot indication of AD. The CT showed no medial manage all his activities of daily living (ADL) temporal atrophy but moderate white matter needs during his episodes of reduced wakeful- changes. Mini mental state examination ness and attention, leading to affected cogni- (MMSE) was initially 27 and is still, almost tion. This means that the level of the disorder is 10 years later, 28. Summarizing these results, I major. ﬁnd it not plausible that the diagnosis is only When the patient ﬁrst came to the Memory AD with normal NFL and the subcortical parts Clinic, Alzheimer’s disease (AD) was suspected, probably not gravely affected. Despite treat- ment, the AD component seems to be small since we cannot catch it in MMSE. It is however Author’s Response to Letter to the Editor by Brzezicki, M., Neurol Ther (2018) https://doi.org/10.1007/s40120- very likely that there is a small AD component 018-0098-8, regarding the article by Londos, E., Neurol since this is more common compared with the Ther (2017) https://doi.org/10.1007/s40120-017-0090-8. opposite in DLB. Differentiation from Parkin- son’s disease dementia (PDD) only depends on Enhanced digital content To view enhanced digital content for this article, go to https://doi.org/10.6084/ the order in which the symptoms appear [3, 5]. m9.ﬁgshare.6097541. Since parkinsonism was the last of the DLB core criteria to appear clinically in the patient, this E. Londos (&) by deﬁnition rules out both Parkinson’s disease Lund University, Skane University Hospital, and PDD. Vascular dementia should also be Institute of Clinical Sciences Malmo ¨ , Clinical considered. The patient had an episode several Memory Research Unit, Malmo ¨ , Sweden e-mail: email@example.com 166 Neurol Ther (2018) 7:165–167 years before he came to the Memory Clinic in orthostatic blood pressure and a depressive which a stroke was suspected, and in an early propensity because of good insight and the CT scan a small infarct in the basal ganglia was patient’s feeling of being a burden to his wife. noted. The symptom at that time was evalu- Also the prompt response to rivastigmine and ated as delirium. However, the description memantine is clinically more common in DLB today by the patient’s wife could lead to sus- compared with AD and vascular dementia. picion of a vascular event. The fact that However, considering the patient’s age, mixed parkinsonism appeared several years after that pathologies are plausible. In my opinion, an LB and is still very mild does not make this infarct pathology is dominant. We can never know for plausible as the cause of the whole clinical sure, but can just be happy knowing that that picture but could, as in many older persons, be the possibility of improvement in these an additive factor. patients exists. I absolutely agree that the treatment we have today can be used in dementias of different origins with positive effects, considering that it ACKNOWLEDGEMENTS is the location rather than the type of pathology that affects the neurotransmitter status in the This response is based on a medical commen- brain. For example, whether the nucleus basalis tary illustrated by a case. of Meynert is affected by a-synuclein, plaques or tangles, it probably leads to lowering of the Funding. No funding or sponsorship was acetyl choline levels. We really do lack suit- received for this study or publication of this able blood and CSF markers to measure the comment. neurotransmitters we hope to affect with our current treatment! As diagnostics work today, Authorship. All named authors meet the we strive to reveal the actual pathology and International Committee of Medical Journal underlying disease for which we do not have Editors (ICMJE) criteria for authorship for this any treatment to offer! article, take responsibility for the integrity of The DLB criteria from 1996  were char- the work as a whole, and have given their acterized by high speciﬁcity but low sensitivity approval for this version to be published. , which contributes to under-recognition. To increase sensitivity, the criteria were revised in Disclosures. Elisabet Londos has nothing to 2005 and 2017 [3, 8]. Also, from my own disclose. clinical perspective from my experience with DLB patients investigated with neuropathol- Compliance with Ethics Guidelines. This ogy, I agree that the criteria are speciﬁc. With article is based on previously conducted studies more core criteria, a higher degree of a-synu- and does not contain any studies with human clein was found in a study by Fujishiro et al. participants or animals performed by any of the . The actual patient had suspected REM authors. sleep behavior disorder with ‘‘wild nightmares’’ and acting out; sometimes the ﬁgures from the Open Access. This article is distributed dreams also appeared in daytime (visual hal- under the terms of the Creative Commons lucinations?), with ﬂuctuating cognition due Attribution-NonCommercial 4.0 International to variations in wakefulness and alertness as License (http://creativecommons.org/licenses/ the most prominent symptom and eventually by-nc/4.0/), which permits any non- mild parkinsonism. This meets four out of four commercial use, distribution, and reproduction core criteria. Further supporting the DLB diag- in any medium, provided you give appropriate nosis in the patient is a cognitive proﬁle with credit to the original author(s) and the source, visuospatial and mathematical difﬁculties provide a link to the Creative Commons license, rather than actual episodic memory problems, and indicate if changes were made. presence of supporting criteria such as Neurol Ther (2018) 7:165–167 167 Parkinson’s disease. Mov Disord. REFERENCES 2007;22(12):1689–707. 1. Brzezicki MA, Kobetic ´ MD. Letter to the editor 6. McKeith IG, Galasko D, Kosaka K, Perry EK, Dickson regarding: practical treatment of Lewy body disease DW, Hansen LA, Salmon DP, Lowe J, Mirra SS, Byrne in the clinic: patient and physician perspectives. EJ, Lennox G, Quinn NP, Edwardson JA, Ince PG, Neurol Ther. 2018. https://doi.org/10.1007/s40120- Bergeron C, Burns A, Miller BL, Lovestone S, Coller- 018-0098-8. ton D, Jansen EN, Ballard C, de Vos RA, Wilcock GK, Jellinger KA, Perry RH. 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Neurology and Therapy – Springer Journals
Published: Apr 27, 2018
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