DOCSLIB.ORG

Diagnosis and Management of Dementia with Lewy Bodies Fourth Consensus Report of the DLB Consortium

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Diagnosis and Management of Dementia with Lewy Bodies Fourth Consensus Report of the DLB Consortium Published Ahead of Print on June 7, 2017 as 10.1212/WNL.0000000000004058 VIEWS & REVIEWS Diagnosis and management of dementia with Lewy bodies Fourth consensus report of the DLB Consortium Ian G. McKeith, MD, ABSTRACT F Med Sci The Dementia with Lewy Bodies (DLB) Consortium has refined its recommendations about the Bradley F. Boeve, MD clinical and pathologic diagnosis of DLB, updating the previous report, which has been in wide- Dennis W. Dickson, MD spread use for the last decade. The revised DLB consensus criteria now distinguish clearly Glenda Halliday, PhD between clinical features and diagnostic biomarkers, and give guidance about optimal methods John-Paul Taylor, PhD, to establish and interpret these. Substantial new information has been incorporated about pre- MRC Psych viously reported aspects of DLB, with increased diagnostic weighting given to REM sleep Daniel Weintraub, MD behavior disorder and 123iodine-metaiodobenzylguanidine (MIBG) myocardial scintigraphy. Dag Aarsland, MD The diagnostic role of other neuroimaging, electrophysiologic, and laboratory investigations James Galvin, MD, MPH is also described. Minor modifications to pathologic methods and criteria are recommended to Johannes Attems, MD take account of Alzheimer disease neuropathologic change, to add previously omitted Lewy- Clive G. Ballard, MRC related pathology categories, and to include assessments for substantia nigra neuronal loss. Psych, MD Recommendations about clinical management are largely based upon expert opinion since Ashley Bayston, BA, LLB randomized controlled trials in DLB are few. Substantial progress has been made since the Thomas G. Beach, MD, previous report in the detection and recognition of DLB as a common and important clinical PhD disorder. During that period it has been incorporated into DSM-5, as major neurocognitive Frédéric Blanc, MD, PhD disorder with Lewy bodies. There remains a pressing need to understand the underlying neu- Nicolaas Bohnen, MD, robiology and pathophysiology of DLB, to develop and deliver clinical trials with both symp- PhD tomatic and disease-modifying agents, and to help patients and carers worldwide to inform Laura Bonanni, MD, themselves about the disease, its prognosis, best available treatments, ongoing research, and PhD how to get adequate support. Neurology® 2017;89:1–13 Jose Bras, PhD Patrick Brundin, MD, GLOSSARY PhD AD 5 Alzheimer disease; CHEI 5 cholinesterase inhibitor; DAT 5 dopamine transporter; DLB 5 dementia with Lewy bodies; David Burn, MD, FRCP DSM-5 5 Diagnostic and Statistical Manual of Mental Disorders, 5th edition; LB 5 Lewy body; MCI 5 mild cognitive impairment; MIBG 5 metaiodobenzylguanidine; MMSE 5 Mini-Mental State Examination; MTL 5 medial temporal lobe; Alice Chen-Plotkin, MD PD 5 Parkinson disease; PSG 5 polysomnography; RBD 5 REM sleep behavior disorder. John E. Duda, MD Omar El-Agnaf, PhD The Dementia with Lewy Bodies (DLB) Consortium last reported on diagnosis and manage- Howard Feldman, MD, ment in December 2005, and its recommendations have been widely cited for both clinical FRCP and research use.1,2 Changes made to the diagnostic criteria at that time increased diagnostic Tanis J. Ferman, PhD sensitivity for DLB,e1 but detection rates in clinical practice remain suboptimal,3 with many Dominic ffytche, MD Hiroshige Fujishiro, MD cases missed or misdiagnosed, usually as Alzheimer disease (AD). The revised DLB criteria Douglas Galasko, MD presented here incorporate new developments since then and result from a review process that Jennifer G. Goldman, combined the reports of 4 multidisciplinary, expert working groups with a meeting that MD, MS included patient and care partner participation (appendix e-1 at Neurology.org). The Consor- Stephen N. Gomperts, tium recognizes increasing interest in detecting early-stage disease; prodromal DLB criteria are in MD, PhD development and will be reported separately. Neill R. Graff-Radford, MD SUMMARY OF CHANGES While maintaining their previous structure, the revised DLB clinical diagnostic Lawrence S. Honig, MD, criteria improve on earlier versions1,2 by distinguishing clearly between clinical features and diagnostic PhD Alex Iranzo, MD, PhD Author affiliations are provided at the end of the article. Members of the DLB Consortium are listed at Neurology.org. Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article. Author list continued on next page The Article Processing Charge was paid by NIHR Newcastle Biomedical Research Centre in Ageing and Long-Term Conditions. This is an open access article distributed under the terms of the Creative Commons Attribution License 4.0 (CC BY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright © 2017 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology. 1 Kejal Kantarci, MD, MS biomarkers, with guidance about optimal methods to e.g., line orientation, size matching tasks; and percep- Daniel Kaufer, MD establish and interpret these. Clinical signs and symp- tual discrimination, e.g., incomplete figures, incom- Walter Kukull, PhD toms are weighted as core or supportive, and bio- plete letters, pareidolia tasks.10,e4 Virginia M.Y. Lee, PhD markers as indicative or supportive, based upon Memory and object naming tend to be less James B. Leverenz, MD their diagnostic specificity and the volume of good- affected in DLB, and are best evaluated through story Simon Lewis, MBBCh, quality evidence available. Although carrying less recall, verbal list learning, and confrontation naming MD diagnostic weight, supportive items are often valuable tasks, although some patients’ difficulties may be sec- Carol Lippa, MD in clinical decision-making, acting as signposts to or ondary to speed or retrieval task demands. Angela Lunde, MA adding evidence for a DLB diagnosis. The previous No DLB-specific assessment batteries have been Mario Masellis, MD, PhD category of suggestive features is no longer used and developed, although recommendations have been Eliezer Masliah, MD those items, namely REM sleep behavior disorder made about suitable existing instruments11 and a com- Pamela McLean, PhD (RBD), severe neuroleptic sensitivity, and low dopa- posite risk score tool has been published.12 Brit Mollenhauer, MD mine transporter (DAT) imaging, have been reas- Core clinical features. Fluctuation. DLB fluctuations Thomas J. Montine, MD, signed in the new scheme. have been described in detail previously1,2 and are PhD The revised criteria (table 1) generate categories typically delirium-like,e5 occurring as spontaneous al- Emilio Moreno, MD, of probable and possible DLB, corresponding to terations in cognition, attention, and arousal. They PhD terminology previously used, describing the clinical include waxing and waning episodes of behavioral Etsuro Mori, MD, PhD presentations most typical of dementia associated inconsistency, incoherent speech, variable attention, Melissa Murray, PhD with underlying Lewy-related pathology. Because or altered consciousness that involves staring or zon- John T. O’Brien, F Med of considerable pathologic heterogeneity, some ing out. Direct questioning of an informant about Sci, DM dementia presentations associated with Lewy-related fluctuations may not reliably discriminate DLB from Sotoshi Orimo, MD, PhD pathology are atypical, e.g., if abundant neocortical AD, but questions about daytime drowsiness, leth- Ronald B. Postuma, MD, neuritic plaques and tangles are present in addition argy, staring into space, or episodes of disorganized MSc to Lewy bodies (LB), the clinical profile may more speech do. These have been incorporated into scales Shankar Ramaswamy, MD closely resemble AD rather than DLB.4,5 Such mixed that either score the severity and frequency of Owen A. Ross, PhD pathology cases are common, explaining why up to fluctuations derived from a clinical interview or use David P. Salmon, PhD half of carefully research-diagnosed patients with informant reports from semi-structured ques- Andrew Singleton, PhD AD may have unsuspected Lewy-related pathology tionnaires.13–16 Recording variations in attentional Angela Taylor, BM at autopsy.6 Criteria for the detection of such pa- performance using repeated computer-based tests Alan Thomas, PhD tients, previously characterized as the LB variant of offers an independent method.e6 At least one measure Pietro Tiraboschi, MD AD,7 remain to be formulated. of fluctuation should be documented when applying Jon B. Toledo, MD, PhD DLB diagnostic criteria. Fluctuations may also occur John Q. Trojanowski, Clinical features. Dementia, defined as a progressive in advanced stages of other dementias, so they best MD, PhD cognitive decline of sufficient magnitude to interfere predict DLB when they are present early.e7 Debby Tsuang, MD with normal social or occupational functions, or with Visual hallucinations. Recurrent, complex visual hallu- Zuzana Walker, MD, usual daily activities, is an essential requirement for cinations occur in up to 80% of patients with DLB FRC Psych DLB diagnosis. and are a frequent clinical signpost to diagnosis. They Masahito Yamada, MD, Although dementia screens such as the Mini- are typically well-formed, featuring people, children, PhD Mental State Examination (MMSE) and Montreal or animals, sometimes accompanied by related phe- Kenji Kosaka, MD Cognitive Assessment are useful to characterize
Load more

Recommended publications
  • Lewy Bodies in the Amygdala Increase of ␣-Synuclein Aggregates in Neurodegenerative Diseases with Tau-Based Inclusions
    ORIGINAL CONTRIBUTION Lewy Bodies in the Amygdala Increase of ␣-Synuclein Aggregates in Neurodegenerative Diseases With Tau-Based Inclusions Anca Popescu, MD; Carol F. Lippa, MD; Virginia M.-Y. Lee, PhD; John Q. Trojanowski, MD, PhD Background: Increased attention has been given to Results: Lewy bodies were often abundant in classic Pick ␣-synuclein aggregation in nonsynucleinopathies be- disease, argyrophilic grain disease, Alzheimer disease, and cause ␣-synuclein–containing Lewy bodies (LBs) influ- dementia with LBs but not in cases with amygdala de- ence symptoms. However, the spectrum of disorders in generation lacking tau-based inclusions, control cases, which secondary inclusions are likely to occur has not preclinical disease carriers, or degenerative diseases lack- been defined. Amygdala neurons commonly develop large ing pathologic involvement of the amygdala. The ex- numbers of secondary LBs, making it a practical region posed ␣-synuclein epitopes were similar in all cases con- for studying this phenomenon. taining LBs. Objective: To characterize the spectrum of diseases as- Conclusions: Abnormal ␣-synuclein aggregation in the sociated with LB formation in the amygdala of neurode- amygdala is disease selective, but not restricted to dis- generative disease and control cases. orders of ␣-synuclein and ␤-amyloid. Our data are com- patible with the notion that tau aggregates predispose neu- Design: An autopsy series of 101 neurodegenerative dis- ease and 34 aged control cases. Using immunohisto- rons to develop secondary LBs. chemistry studies, we examined the amygdala for ␣-synuclein aggregates. Arch Neurol. 2004;61:1915-1919 GGREGATION OF ␣-SY- of these subjects.7-9 It is unknown whether nuclein has a primary this curious finding is restricted to AD, or pathogenic role in spo- whether it is a more universal phenom- radic and familial autoso- enon.
    [Show full text]
  • Lewy Body Dementias: a Coin with Two Sides?
    behavioral sciences Review Lewy Body Dementias: A Coin with Two Sides? Ángela Milán-Tomás 1 , Marta Fernández-Matarrubia 2,3 and María Cruz Rodríguez-Oroz 1,2,3,4,* 1 Department of Neurology, Clínica Universidad de Navarra, 28027 Madrid, Spain; [email protected] 2 Department of Neurology, Clínica Universidad de Navarra, 31008 Pamplona, Spain; [email protected] 3 IdiSNA, Navarra Institute for Health Research, 31008 Pamplona, Spain 4 CIMA, Center of Applied Medical Research, Universidad de Navarra, Neurosciences Program, 31008 Pamplona, Spain * Correspondence: [email protected] Abstract: Lewy body dementias (LBDs) consist of dementia with Lewy bodies (DLB) and Parkin- son’s disease dementia (PDD), which are clinically similar syndromes that share neuropathological findings with widespread cortical Lewy body deposition, often with a variable degree of concomitant Alzheimer pathology. The objective of this article is to provide an overview of the neuropathological and clinical features, current diagnostic criteria, biomarkers, and management of LBD. Literature research was performed using the PubMed database, and the most pertinent articles were read and are discussed in this paper. The diagnostic criteria for DLB have recently been updated, with the addition of indicative and supportive biomarker information. The time interval of dementia onset relative to parkinsonism remains the major distinction between DLB and PDD, underpinning controversy about whether they are the same illness in a different spectrum of the disease or two separate neurodegenerative disorders. The treatment for LBD is only symptomatic, but the expected progression and prognosis differ between the two entities. Diagnosis in prodromal stages should be of the utmost importance, because implementing early treatment might change the course of the Citation: Milán-Tomás, Á.; illness if disease-modifying therapies are developed in the future.
    [Show full text]
  • Sleep Environment and Non-Rapid Eye Movement-Related Parasomnia Among Children: 42 Case Series
    pISSN 2093-9175 / eISSN 2233-8853 BRIEF COMMUNICATION https://doi.org/10.17241/smr.2020.00535 Sleep Environment and Non-Rapid Eye Movement-Related Parasomnia Among Children: 42 Case Series Joohee Lee, MD, Sungook Yeo, MD, Kyumin Kim, MD, Seockhoon Chung, MD, PhD Department of Psychiatry, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea The purpose of this study was to identify the clinical features related to sleep environment of non- rapid eye movement (NREM)-related parasomnia. It was a retrospective medical record review of 42 children. We investigated demographic information, sleep pattern, sleep environment, and the mother’s dysfunctional beliefs about the child’s sleep. The mean age of subjects was 6.3± 3.1. The diagnosis was night terror (n = 21), sleepwalking (n = 8), confusional arousal (n = 2), and unspeci- fied (n = 11). The average time of sleep pattern was as follow; bedtime 21:39± 0:54 pm, sleep onset time 22:13 ± 0:54 pm, wake-up time 7:37 ± 0:42 am and NREM-related parasomnia occurrence time 1:09 ± 2:04 am. The average number of co-sleeping members was 2.8. 48.5% (n = 16) mothers experienced coldness while sleeping, and 64.7% (n = 22) parents had dysfunctional beliefs about their children’s sleep. The large number of co-sleeping members, coldness mothers experienced while sleeping, and dysfunctional beliefs about their children’s sleep may influence the NREM-pa- rasomnia in children. Sleep Med Res 2020;11(1):49-52 Key WordsaaParasomnia, Sleep environment, Co-sleep, Children. INTRODUCTION Received: April 3, 2020 A significant number of children are impacted by sleep disorders, reported in 25–62% of Revised: April 27, 2020 Accepted: May 4, 2020 such children [1,2].
    [Show full text]
  • PTSD and Sleep Corporal Michael J
    VOLUME 27/NO. 4 • ISSN: 1050-1835 • 2016 Research Quarterly advancing science and promoting understanding of traumatic stress Published by: Philip Gehrman, PhD National Center for PTSD University of Pennsylvania, Department of Psychiatry VA Medical Center (116D) 215 North Main Street Gerlinde Harb, PhD White River Junction Estadt Psychological Services and Vermont 05009-0001 USA PTSD and Sleep Corporal Michael J. Crescenz VA Medical Center (802) 296-5132 Richard Ross, MD, PhD FAX (802) 296-5135 Department of Veterans Affairs Medical Center and Email: [email protected] University of Pennsylvania, Department of Psychiatry All issues of the PTSD Research Quarterly are available online at: www.ptsd.va.gov Introduction Study, 52% of combat Veterans with PTSD reported a significant nightmare problem (Neylan et al., 1998). Editorial Members: PTSD is unique among mental health disorders in In a general community sample, nightmares were Editorial Director that sleep problems represent two of the diagnostic endorsed by 71% of individuals with PTSD (Leskin, Matthew J. Friedman, MD, PhD criteria of the fifth edition of the American Psychiatric Woodward, Young, & Sheikh, 2002). Posttraumatic Bibliographic Editor Association’s (APA) Diagnostic and Statistical Manual nightmares are independently associated with Misty Carrillo, MLIS of Mental Disorders (DSM-5); recurrent nightmares daytime distress and impaired functioning over and Managing Editor are part of the intrusion cluster of symptoms, and above the impact of overall PTSD severity (Levin & Heather Smith, BA Ed insomnia is a component of the arousal cluster. Nielsen, 2007; Littlewood, Gooding, Panagioti, & While these sleep problems are symptoms of PTSD, Kyle, 2016). National Center Divisions: the evidence suggests that they tend to become Executive independent problems over time, warranting sleep- Insomnia and recurrent nightmares are traditionally White River Jct VT focused assessment and treatment.
    [Show full text]
  • Clinical, Neuropathological and Genetic Features of Lewy Body Dementias
    Clinical, neuropathological and genetic features of Lewy body dementias Hansen D¹, Ling H¹ʹ², Lashley T², Holton JL², Warner TT¹ʹ² ¹Reta Lila Weston Institute, UCL Queen Square Institute of Neurology, London ²Queen Square Brain Bank for Neurological Disorders, UCL Queen Square Institute of Neurology, London Abstract: Lewy body dementias are the second most common neurodegenerative dementias after Alzheimer’s disease, and include dementia with Lewy bodies and Parkinson’s disease dementia. They share similar clinical and neuropathological features but differ in the time of dementia and parkinsonism onset. Although Lewy bodies are their main pathological hallmark, several studies have shown the emerging importance of Alzheimer’s disease pathology. Clinical amyloid-β imaging using Pittsburgh Compound B (PiB) supports neuropathological studies which found that amyloid-β pathology is more common in dementia with Lewy bodies than in Parkinson’s disease dementia. Nevertheless, other co-occurring pathologies, such as cerebral amyloid angiopathy, TDP-43 pathology and synaptic pathology may also influence the development of neurodegeneration and dementia. Recent genetic studies demonstrated an important role of APOE genotype, and other genes such as GBA and SNCA which seem to be involved in the pathophysiology of Lewy body dementias. The aim of this article is to review the main clinical, neuropathological and genetic aspects of dementia with Lewy bodies and Parkinson’s disease dementia. This is particularly relevant as future management for these
    [Show full text]
  • Epileptic Mechanisms Shared by Alzheimer's Disease
    International Journal of Molecular Sciences Review Epileptic Mechanisms Shared by Alzheimer’s Disease: Viewed via the Unique Lens of Genetic Epilepsy Jing-Qiong Kang 1,2 1 Department of Neurology & Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232-8552, USA; [email protected]; Tel.: +1-615-936-8399; Fax: +1-615-322-5517 2 Vanderbilt Kennedy Center of Human Development, Vanderbilt Brain Institute, Vanderbilt University, Nashville, TN 37232-8522, USA Abstract: Our recent work on genetic epilepsy (GE) has identified common mechanisms between GE and neurodegenerative diseases including Alzheimer’s disease (AD). Although both disorders are seemingly unrelated and occur at opposite ends of the age spectrum, it is likely there are shared mechanisms and studies on GE could provide unique insights into AD pathogenesis. Neurodegen- erative diseases are typically late-onset disorders, but the underlying pathology may have already occurred long before the clinical symptoms emerge. Pathophysiology in the early phase of these diseases is understudied but critical for developing mechanism-based treatment. In AD, increased seizure susceptibility and silent epileptiform activity due to disrupted excitatory/inhibitory (E/I) balance has been identified much earlier than cognition deficit. Increased epileptiform activity is likely a main pathology in the early phase that directly contributes to impaired cognition. It is an enormous challenge to model the early phase of pathology with conventional AD mouse models due to the chronic disease course, let alone the complex interplay between subclinical nonconvulsive epileptiform activity, AD pathology, and cognition deficit. We have extensively studied GE, especially with gene mutations that affect the GABA pathway such as mutations in GABAA receptors and GABA transporter Citation: Kang, J.-Q.
    [Show full text]
  • When DLB, PD, and PSP Masquerade As MSA an Autopsy Study of 134 Patients
    When DLB, PD, and PSP masquerade as MSA An autopsy study of 134 patients Shunsuke Koga, MD ABSTRACT Naoya Aoki, MD Objective: To determine ways to improve diagnostic accuracy of multiple system atrophy (MSA), Ryan J. Uitti, MD we assessed the diagnostic process in patients who came to autopsy with antemortem diagnosis Jay A. van Gerpen, MD of MSA by comparing clinical and pathologic features between those who proved to have MSA William P. Cheshire, MD and those who did not. We focus on likely explanations for misdiagnosis. Keith A. Josephs, MD Methods: This is a retrospective review of 134 consecutive patients with an antemortem clinical Zbigniew K. Wszolek, diagnosis of MSA who came to autopsy with neuropathologic evaluation of the brain. Of the 134 MD patients, 125 had adequate medical records for review. Clinical and pathologic features were J. William Langston, MD compared between patients with autopsy-confirmed MSA and those with other pathologic diag- Dennis W. Dickson, MD noses, including dementia with Lewy bodies (DLB), Parkinson disease (PD), and progressive supra- nuclear palsy (PSP). Correspondence to Results: Of the 134 patients with clinically diagnosed MSA, 83 (62%) had the correct diagnosis Dr. Dickson: at autopsy. Pathologically confirmed DLB was the most common misdiagnosis, followed by PSP [email protected] and PD. Despite meeting pathologic criteria for intermediate to high likelihood of DLB, several pa- tients with DLB did not have dementia and none had significant Alzheimer-type pathology. Auto- nomic failure was the leading cause of misdiagnosis in DLB and PD, and cerebellar ataxia was the leading cause of misdiagnosis in PSP.
    [Show full text]
  • Dementia with Lewy Bodies
    Dementia with Lewy Bodies David Gill, MD, FAAN Chair, Department of Neurology Director, Memory Center at Unity Unity Hospital Dr. Gill has no conflicts or professional relationships to disclose. Learning objectives Overview of parkinsonian dementias Diagnosis of dementia with Lewy bodies Pathophysiology of dementia with Lewy bodies Treatment 3 Sam John Joan Estimated causes of dementia Alzheimer's disease Mixed causes Vascular Dementia Lewy Body Dementias Frontotemporal Lobar Degenerations Unknown Other Classification of Cognitive Disorders Motor neuron Tardopathies Comportment Movement Disorders LATE? ALS limbic-predominate FTD Synucleinopathies age related TDP-43 MSA encephalopathy PD Semantic HD Tauopathies PSP CBD DLB Amyloidopathies PPA AD Amnestic Language ALS = amyotrophic lateral sclerosis; FTD = frontotemporal dementia; MSA = multisystem atrophy; Semantic = semantic dementia; PD = Parkinson’s disease; HD = Huntingdon’s disease; PSP = progressive supranuclear palsy; CBD = corticobasal degeneration; DLB = dementia with Lewy bodies; PPA = primary progressive aphasia; AD = Alzheimer’s disease Parkinsonian dementias Slowness of movement, tremor, and cognitive impairment. Dementia with Lewy Bodies Generally do not respond well to carbidopa/levodopa Parkinson’s disease with Same as dementia with Lewy bodies, but cognitive symptoms Lewy bodies dementia start one year or more after parkinsonism Slowness of movement, tremor and cognitive impairment along with lightheadedness when standing up and trouble controlling 2007 . Multisystem atrophy bladder. Generally also does not respond well to Clin carbidopa/levodopa Wide-eyed stare, reduced eye blink frequency, back and neck Progressive Supranuclear Neurol stiffness. Generally also does not respond well to Palsy B. , carbidopa/levodopa Slowness of movement, tremor as well as stiffness, jerking Tau-opathies Corticobasal syndrome movements and alien limb.
    [Show full text]
  • Cognitive Behavioral Therapy for Insomnia Enhances Depression Outcome in Patients with Comorbid Major Depressive Disorder and Insomnia
    INSOMNIA AND DEPRESSION Cognitive Behavioral Therapy for Insomnia Enhances Depression Outcome in Patients with Comorbid Major Depressive Disorder and Insomnia Rachel Manber, PhD1; Jack D. Edinger, PhD2; Jenna L. Gress, BA1; Melanie G. San Pedro-Salcedo, MA1; Tracy F. Kuo, PhD1; Tasha Kalista, MA1 1Stanford University, Stanford, CA; 2VA Medical Center and Duke University Medical Center, Durham, NC Study Objective: Insomnia impacts the course of major depressive severity index (ISI), daily sleep diaries, and actigraphy. disorder (MDD), hinders response to treatment, and increases risk for EsCIT + CBTI resulted in a higher rate of remission of depression depressive relapse. This study is an initial evaluation of adding cogni- (61.5%) than EsCIT + CTRL (33.3%). EsCIT + CBTI was also associat- tive behavioral therapy for insomnia (CBTI) to the antidepressant medi- ed with a greater remission from insomnia (50.0%) than EsCIT + CTRL cation escitalopram (EsCIT) in individuals with both disorders. (7.7%) and larger improvement in all diary and actigraphy measures of Design and setting: A randomized, controlled, pilot study in a single sleep, except for total sleep time. academic medical center. Conclusion: This pilot study provides evidence that augmenting an Participants: 30 individuals (61% female, mean age 35±18) with MDD antidepressant medication with a brief, symptom focused, cognitive- and insomnia. behavioral therapy for insomnia is promising for individuals with MDD Interventions: EsCIT and 7 individual therapy sessions of CBTI or and comorbid insomnia in terms of alleviating both depression and in- CTRL (quasi-desensitization). somnia. Measurements and results: Depression was assessed with the Keywords: Major depressive disorder, Insomnia, Cognitive behavioral HRSD17 and the depression portion of the SCID, administered by raters therapy, Remission masked to treatment assignment, at baseline and after 2, 4, 6, 8, and Citation: Manber R; Edinger JD; Gress JL; San Pedro-Salcedo MG; 12 weeks of treatment.
    [Show full text]
  • Parasomnias and Antidepressant Therapy: a Review of the Literature
    REVIEW ARTICLE published: 12 December 2011 PSYCHIATRY doi: 10.3389/fpsyt.2011.00071 Parasomnias and antidepressant therapy: a review of the literature Lara Kierlin1,2 and Michael R. Littner 1,2* 1 David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA, USA 2 Pulmonary, Critical Care and Sleep Medicine, VA Greater Los Angeles Healthcare System, Los Angeles, CA, USA Edited by: There exists a varying level of evidence linking the use of antidepressant medication to Ruth Benca, University of the parasomnias, ranging from larger, more comprehensive studies in the area of REM Wisconsin – Madison School of Medicine, USA sleep behavior disorder to primarily case reports in the NREM parasomnias. As such, prac- Reviewed by: tice guidelines are lacking regarding specific direction to the clinician who may be faced Ruth Benca, University of with a patient who has developed a parasomnia that appears to be temporally related to Wisconsin – Madison School of use of an antidepressant. In general, knowledge of the mechanisms of action of the med- Medicine, USA ications, particularly with regard to the impact on sleep architecture, can provide some David Plante, University of Wisconsin, USA guidance. There is a potential for selective serotonin reuptake inhibitors, tricyclic antide- *Correspondence: pressants, and serotonin–norepinephrine reuptake inhibitors to suppress REM, as well Michael R. Littner, 10736 Des Moines as the anticholinergic properties of the individual drugs to further disturb normal sleep Avenue, Porter Ranch, Los Angeles, architecture. CA 91326, USA. e-mail: [email protected] Keywords: parasomnias, REM sleep behavior disorder, non-REM parasomnias, selective serotonin reuptake inhibitors, depression INTRODUCTION and night terrors (Ohayon et al., 1999; Yeh et al., 2009).
    [Show full text]
  • Lewy Body Diseases and Multiple System Atrophy As ␣-Synucleinopathies
    Molecular Psychiatry (1998) 3, 462–465 1998 Stockton Press All rights reserved 1359–4184/98 $12.00 GUEST EDITORIAL Lewy body diseases and multiple system atrophy as ␣-synucleinopathies Parkinson’s disease and dementia with Lewy bodies synuclein are the first known genetic causes of Parkin- are among the most common neurodegenerative dis- son’s disease. They are located in the amino-terminal eases. They share the Lewy body and the Lewy neurite half of ␣-synuclein, which consists of seven imperfect as their defining neuropathological characteristics. repeats of 11 amino acids each, with the consensus Originally described in 1912 as a light-microscopic sequence KTKEGV (Figure 1). It has been suggested entity, the Lewy body was shown to be made of abnor- that ␣-synuclein may bind through these repeats to mal filaments in the 1960s. Over the past year, the bio- membranes rich in acidic phospholipids.3 chemical nature of the Lewy body filament has been This work raised the question whether ␣-synuclein revealed. is a component of Lewy bodies and Lewy neurites of A large number of different proteins has been idiopathic Parkinson’s disease and of dementia with reported to be present in Lewy bodies and Lewy neur- Lewy bodies. Using well-characterised anti-␣-synuc- ites by immunohistochemical methods. However, these lein antibodies, Spillantini et al showed strong staining findings do not permit us to distinguish between of both Lewy bodies and Lewy neurites in idiopathic intrinsic Lewy body components and normal cellular Parkinson’s disease and dementia with Lewy bodies.4 constituents that get merely trapped in the filaments They also reported the lack of staining of these patho- that make up the Lewy body.
    [Show full text]
  • The Co-Occurrence of Sexsomnia, Sleep Bruxism and Other Sleep Disorders
    Journal of Clinical Medicine Review The Co-Occurrence of Sexsomnia, Sleep Bruxism and Other Sleep Disorders Helena Martynowicz 1, Joanna Smardz 2, Tomasz Wieczorek 3, Grzegorz Mazur 1, Rafal Poreba 1, Robert Skomro 4, Marek Zietek 5, Anna Wojakowska 1, Monika Michalek 1 ID and Mieszko Wieckiewicz 2,* 1 Department of Internal Medicine, Occupational Diseases and Hypertension, Wroclaw Medical University, 50-367 Wroclaw, Poland; [email protected] (H.M.); [email protected] (G.M.); [email protected] (R.P.); [email protected] (A.W.); [email protected] (M.M.) 2 Department of Experimental Dentistry, Wroclaw Medical University, 50-367 Wroclaw, Poland; [email protected] 3 Department and Clinic of Psychiatry, Wroclaw Medical University, 50-367 Wroclaw, Poland; [email protected] 4 Division of Respiratory Critical Care and Sleep Medicine, Department of Medicine, University of Saskatchewan, Saskatoon, SK S7N 5A2, Canada; [email protected] 5 Department of Periodontology, Wroclaw Medical University, 50-367 Wroclaw, Poland; [email protected] * Correspondence: [email protected]; Tel.: +48-660-47-87-59 Received: 3 August 2018; Accepted: 19 August 2018; Published: 23 August 2018 Abstract: Background: Sleep sex also known as sexsomnia or somnambulistic sexual behavior is proposed to be classified as NREM (non-rapid eye movement) parasomnia (as a clinical subtype of disorders of arousal from NREM sleep—primarily confusional arousals or less commonly sleepwalking), but it has also been described in relation to REM (rapid eye movement) parasomnias. Methods: The authors searched the PubMed database to identify relevant publications and present the co-occurrence of sexsomnia and other sleep disorders as a non-systematic review with case series.
    [Show full text]