Author’s Response to the Letter to the Editor Regarding: Practical Treatment of Lewy Body Disease in the Clinic: Patient and Physician Perspectives

Author’s Response to the Letter to the Editor Regarding: Practical Treatment of Lewy Body... 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 [1] comments on the probably because his main complaint was for- case of a patient with Lewy Body Dementia [2] 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 [3] 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) [4]. 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: elisabet.londos@skane.se 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 [6] 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. [7], 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 [9]. 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. Consensus guidelines for the 2. Londos E. Practical treatment of Lewy body disease in clinical and pathologic diagnosis of dementia with the clinic: patient and physician perspectives. Neurol Lewy bodies (DLB): report of the consortium on DLB Ther. 2017. https://doi.org/10.1007/s40120-017- international workshop. Neurology. 0090-8. 1996;47(5):1113–24. 3. McKeith IG, Boeve BF, Dickson DW, Halliday G, 7. Rizzo G, Arcuti S, Copetti M, Alessandria M, Savica R, Taylor JP, Weintraub D, Aarsland D, Galvin J, Attems Fontana A, Liguori R, Logroscino G. Accuracy of J, Ballard CG, Bayston A, Beach TG, Blanc F, Bohnen clinical diagnosis of dementia with Lewy bodies: a N, Bonanni L, Bras J, Brundin P, Burn D, Chen-Plotkin systematic review and meta-analysis. J Neurol Neuro- A, Duda JE, El-Agnaf O, Feldman H, Ferman TJ, surg Psychiatry. 2018;89:358–66. Ffytche D, Fujishiro H, Galasko D, Goldman JG, Gomperts SN, Graff-Radford NR, Honig LS, Iranzo A, 8. McKeith IG, Dickson DW, Lowe J, Emre M, O’Brien Kantarci K, Kaufer D, Kukull W, Lee VMY, Leverenz JT, Feldman H, Cummings J, Duda JE, Lippa C, Perry JB, Lewis S, Lippa C, Lunde A, Masellis M, Masliah E, EK, Aarsland D, Arai H, Ballard CG, Boeve B, Burn DJ, McLean P, Mollenhauer B, Montine TJ, Moreno E, Costa D, Del Ser T, Dubois B, Galasko D, Gauthier S, Mori E, Murray M, O’Brien JT, Orimo S, Postuma RB, Goetz CG, Gomez-Tortosa E, Halliday G, Hansen LA, Hardy J, Iwatsubo T, Kalaria RN, Kaufer D, Kenny RA, Ramaswamy S, Ross OA, Salmon DP, Singleton A, Korczyn A, Kosaka K, Lee VM, Lees A, Litvan I, Londos Taylor A, Thomas A, Tiraboschi P, Toledo JB, Tro- E, Lopez OL, Minoshima S, Mizuno Y, Molina JA, janowski JQ, Tsuang D, Walker Z, Yamada M, Kosaka Mukaetova-Ladinska EB, Pasquier F, Perry RH, Schulz K. Diagnosis and management of dementia with Lewy JB, Trojanowski JQ, Yamada M, Consortium on DLB. bodies: fourth consensus report of the DLB consor- Diagnosis and management of dementia with Lewy tium. Neurology. 2017;89(1):88–100. bodies: third report of the DLB consortium. Neurol- ogy. 2005;65(12):1863–72. 4. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 5th ed. Arling- 9. Fujishiro H, Ferman TJ, Boeve BF, Smith GE, Graff- ton: American Psychiatric Association; 2013. Radford NR, Uitti RJ, Wszolek ZK, Knopman DS, Petersen RC, Parisi JE, Dickson DW. Validation of the 5. Emre M, Aarsland D, Brown R, Burn DJ, Duyckaerts C, neuropathologic criteria of the third consortium for Mizuno Y, Broe GA, Cummings J, Dickson DW, Gauthier S, Goldman J, Goetz C, Korczyn A, Lees A, dementia with Lewy bodies for prospectively diag- Levy R, Litvan I, McKeith I, Olanow W, Poewe W, nosed cases. J Neuropathol Exp Neurol. Quinn N, Sampaio C, Tolosa E, Dubois B. Clinical 2008;67(7):649–56. diagnostic criteria for dementia associated with http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neurology and Therapy Springer Journals

Author’s Response to the Letter to the Editor Regarding: Practical Treatment of Lewy Body Disease in the Clinic: Patient and Physician Perspectives

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Abstract

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 [1] comments on the probably because his main complaint was for- case of a patient with Lewy Body Dementia [2] 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 [3] 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) [4]. 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: elisabet.londos@skane.se 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 [6] 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. [7], 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 [9]. 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. Consensus guidelines for the 2. Londos E. Practical treatment of Lewy body disease in clinical and pathologic diagnosis of dementia with the clinic: patient and physician perspectives. Neurol Lewy bodies (DLB): report of the consortium on DLB Ther. 2017. https://doi.org/10.1007/s40120-017- international workshop. Neurology. 0090-8. 1996;47(5):1113–24. 3. McKeith IG, Boeve BF, Dickson DW, Halliday G, 7. Rizzo G, Arcuti S, Copetti M, Alessandria M, Savica R, Taylor JP, Weintraub D, Aarsland D, Galvin J, Attems Fontana A, Liguori R, Logroscino G. Accuracy of J, Ballard CG, Bayston A, Beach TG, Blanc F, Bohnen clinical diagnosis of dementia with Lewy bodies: a N, Bonanni L, Bras J, Brundin P, Burn D, Chen-Plotkin systematic review and meta-analysis. J Neurol Neuro- A, Duda JE, El-Agnaf O, Feldman H, Ferman TJ, surg Psychiatry. 2018;89:358–66. Ffytche D, Fujishiro H, Galasko D, Goldman JG, Gomperts SN, Graff-Radford NR, Honig LS, Iranzo A, 8. McKeith IG, Dickson DW, Lowe J, Emre M, O’Brien Kantarci K, Kaufer D, Kukull W, Lee VMY, Leverenz JT, Feldman H, Cummings J, Duda JE, Lippa C, Perry JB, Lewis S, Lippa C, Lunde A, Masellis M, Masliah E, EK, Aarsland D, Arai H, Ballard CG, Boeve B, Burn DJ, McLean P, Mollenhauer B, Montine TJ, Moreno E, Costa D, Del Ser T, Dubois B, Galasko D, Gauthier S, Mori E, Murray M, O’Brien JT, Orimo S, Postuma RB, Goetz CG, Gomez-Tortosa E, Halliday G, Hansen LA, Hardy J, Iwatsubo T, Kalaria RN, Kaufer D, Kenny RA, Ramaswamy S, Ross OA, Salmon DP, Singleton A, Korczyn A, Kosaka K, Lee VM, Lees A, Litvan I, Londos Taylor A, Thomas A, Tiraboschi P, Toledo JB, Tro- E, Lopez OL, Minoshima S, Mizuno Y, Molina JA, janowski JQ, Tsuang D, Walker Z, Yamada M, Kosaka Mukaetova-Ladinska EB, Pasquier F, Perry RH, Schulz K. Diagnosis and management of dementia with Lewy JB, Trojanowski JQ, Yamada M, Consortium on DLB. bodies: fourth consensus report of the DLB consor- Diagnosis and management of dementia with Lewy tium. Neurology. 2017;89(1):88–100. bodies: third report of the DLB consortium. Neurol- ogy. 2005;65(12):1863–72. 4. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 5th ed. Arling- 9. Fujishiro H, Ferman TJ, Boeve BF, Smith GE, Graff- ton: American Psychiatric Association; 2013. Radford NR, Uitti RJ, Wszolek ZK, Knopman DS, Petersen RC, Parisi JE, Dickson DW. Validation of the 5. Emre M, Aarsland D, Brown R, Burn DJ, Duyckaerts C, neuropathologic criteria of the third consortium for Mizuno Y, Broe GA, Cummings J, Dickson DW, Gauthier S, Goldman J, Goetz C, Korczyn A, Lees A, dementia with Lewy bodies for prospectively diag- Levy R, Litvan I, McKeith I, Olanow W, Poewe W, nosed cases. J Neuropathol Exp Neurol. Quinn N, Sampaio C, Tolosa E, Dubois B. Clinical 2008;67(7):649–56. diagnostic criteria for dementia associated with

Journal

Neurology and TherapySpringer Journals

Published: Apr 27, 2018

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