scholarly journals Acute treatment of psychotic symptoms in a newly diagnosed Lewy body dementia patient with an accelerated titration schedule of rivastigmine and de-escalation of antipsychotics

2019 ◽  
Vol 12 (9) ◽  
pp. e230193 ◽  
Author(s):  
Rebecca Nicole Burgett ◽  
Thomas Michael Farley ◽  
Lori Ann Beireis
Keyword(s):  
Lewy Body ◽  
Low Dose ◽  
Medication Management ◽  
Lewy Body Dementia ◽  
Psychotic Symptoms ◽  
Dementia Patient ◽  
Alternative Treatment Strategy ◽  
Days Of Therapy ◽  
Titration Schedule ◽  
Chei Therapy

A 76-year-old man presented with complaints of increased confusion, visual hallucinations and decline in memory. He was admitted to the hospital and started on quetiapine 50 mg daily for symptom management. Shortly after, he was diagnosed with Lewy body dementia and started on rivastigmine, a cholinesterase inhibitor (ChEI), at 1.5 mg two times per day. The patient’s symptoms continued to worsen and antipsychotics increased for aggressive behaviour. After he became physically aggressive, an extensive medication management review was conducted, prompting an alternative treatment strategy. The quetiapine dose was reduced from 150 mg daily to 12.5 mg daily, his rivastigmine was increased to 3 mg two times per day and all other antipsychotics were discontinued. The up-titration of his rivastigmine after 10 days of therapy was well tolerated with no adverse effects. He demonstrated a clear clinical response to optimised ChEI therapy and low dose quetiapine, showing improvements in alertness and functioning.

scholarly journals Diagnosis and management of Alzheimer's disease

2000 ◽  
Vol 2 (2) ◽  
pp. 129-138
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Activities Of Daily Living ◽  
Vascular Dementia ◽  
Lewy Body ◽  
Daily Living ◽  
Memory Loss ◽  
Lewy Body Dementia ◽  
Psychotic Symptoms ◽  
Dementia Syndrome

The diagnosis of Alzheimer's disease (AD) is a 2-stage process, in stage 1, the dementia syndrome, comprising neuropsychologic and neuropsychiatrie components together with deficits in activities of daily living, is differentiated on clinical grounds from a number of other conditions (delirium, concomitant physical illness, drug treatment normal memory loss, etc), in stage 2, the cause is determined, AD being the most common, followed by vascular dementia, Lewy-body dementia, frontal lobe dementia, and a host of so-called secondary causes. Although a mixed Alzheimer/vascular picture is common, gradual onset of multiple cognitive deficits is typical of AD, while abrupt onset, a fluctuating course, hypertension, and focal neurologic signs suggest vascular dementia, in Lewy-body dementia, memory loss may not be an early feature, and fluctuation can be marked by distressing psychotic symptoms and behavioral disturbance, investigations should be minimally invasive and relatively cheap, confined to routine blood tests, chest x-ray and/or electrocardiogram if clinically indicated, cardiologie or neurologic referral in the presence of cerebrovascular signs, and computed tomography if an intracranial lesion is suspected. Accurate diagnosis enables the clinician to outline the disease course to the family and inform them of genetic implications. Numerous instruments for assessing cognitive function, global status, psychiatric well-being, and activities of daily living are briefly reviewed.

Lewy Body Dementia

2005 ◽  
Vol 10 (2) ◽  
pp. 7-10 ◽  
Author(s):  
Susan Goldfein ◽  
Constance Dean Qualls
Keyword(s):  
Lewy Body ◽  
Lewy Body Dementia

scholarly journals Cross-platform transcriptional profiling identifies common and distinct molecular pathologies in Lewy body diseases

2021 ◽  
Author(s):  
Rahel Feleke ◽  
Regina H. Reynolds ◽  
Amy M. Smith ◽  
Bension Tilley ◽  
Sarah A. Gagliano Taliun ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Diseases ◽  
Lewy Body ◽  
Molecular Mechanisms ◽  
Lewy Bodies ◽  
Subsequent Development ◽  
Lewy Body Dementia ◽  
Anterior Cingulate ◽  
Lewy Body Diseases

AbstractParkinson’s disease (PD), Parkinson’s disease with dementia (PDD) and dementia with Lewy bodies (DLB) are three clinically, genetically and neuropathologically overlapping neurodegenerative diseases collectively known as the Lewy body diseases (LBDs). A variety of molecular mechanisms have been implicated in PD pathogenesis, but the mechanisms underlying PDD and DLB remain largely unknown, a knowledge gap that presents an impediment to the discovery of disease-modifying therapies. Transcriptomic profiling can contribute to addressing this gap, but remains limited in the LBDs. Here, we applied paired bulk-tissue and single-nucleus RNA-sequencing to anterior cingulate cortex samples derived from 28 individuals, including healthy controls, PD, PDD and DLB cases (n = 7 per group), to transcriptomically profile the LBDs. Using this approach, we (i) found transcriptional alterations in multiple cell types across the LBDs; (ii) discovered evidence for widespread dysregulation of RNA splicing, particularly in PDD and DLB; (iii) identified potential splicing factors, with links to other dementia-related neurodegenerative diseases, coordinating this dysregulation; and (iv) identified transcriptomic commonalities and distinctions between the LBDs that inform understanding of the relationships between these three clinical disorders. Together, these findings have important implications for the design of RNA-targeted therapies for these diseases and highlight a potential molecular “window” of therapeutic opportunity between the initial onset of PD and subsequent development of Lewy body dementia.

scholarly journals Functional connectivity of the nucleus basalis of Meynert in Lewy body dementia and Alzheimer’s disease

2021 ◽  
pp. 1-6
Author(s):  
Julia Schumacher ◽  
Alan J. Thomas ◽  
Luis R. Peraza ◽  
Michael Firbank ◽  
John T. O’Brien ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Functional Connectivity ◽  
Lewy Body ◽  
Cholinergic System ◽  
Structural Changes ◽  
Lewy Body Dementia ◽  
Occipital Cortex ◽  
Nucleus Basalis ◽  
Nucleus Basalis Of Meynert

ABSTRACT Cholinergic deficits are a hallmark of Alzheimer’s disease (AD) and Lewy body dementia (LBD). The nucleus basalis of Meynert (NBM) provides the major source of cortical cholinergic input; studying its functional connectivity might, therefore, provide a tool for probing the cholinergic system and its degeneration in neurodegenerative diseases. Forty-six LBD patients, 29 AD patients, and 31 healthy age-matched controls underwent resting-state functional magnetic resonance imaging (fMRI). A seed-based analysis was applied with seeds in the left and right NBM to assess functional connectivity between the NBM and the rest of the brain. We found a shift from anticorrelation in controls to positive correlations in LBD between the right/left NBM and clusters in right/left occipital cortex. Our results indicate that there is an imbalance in functional connectivity between the NBM and primary visual areas in LBD, which provides new insights into alterations within a part of the corticopetal cholinergic system that go beyond structural changes.

Characterization of dementia with Lewy bodies (DLB) and mild cognitive impairment using the Lewy body dementia module (LBD‐MOD)

2021 ◽  
Author(s):  
James E. Galvin ◽  
Stephanie Chrisphonte ◽  
Iris Cohen ◽  
Keri K. Greenfield ◽  
Michael J. Kleiman ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Lewy Body ◽  
Dementia With Lewy Bodies ◽  
Lewy Bodies ◽  
Lewy Body Dementia

scholarly journals The individual course of neuropsychiatric symptoms in people with Alzheimer's and Lewy body dementia: 12-year longitudinal cohort study

2019 ◽  
Vol 216 (1) ◽  
pp. 43-48 ◽  
Author(s):  
Audun Osland Vik-Mo ◽  
Lasse Melvaer Giil ◽  
Miguel Germán Borda ◽  
Clive Ballard ◽  
Dag Aarsland
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neuropsychiatric Symptoms ◽  
Personalised Medicine ◽  
Lewy Bodies ◽  
Lewy Body Dementia ◽  
Psychotic Symptoms ◽  
Primary Inclusion ◽  
The Individual

IntroductionUnderstanding the natural course of neuropsychiatric symptoms (NPS) in dementia is important for planning patient care and trial design, but few studies have described the long-term course of NPS in individuals.MethodPrimary inclusion of 223 patients with suspected mild dementia from general practice were followed by annual assessment, including the Neuropsychiatric Inventory (NPI), for up to 12 years. Total and item NPI scores were classified as stable, relapsing, single episodic or not present based on 4.96 (s.d. 2.3) observations (98% completeness of longitudinal data) for 113 patients with Alzheimer's disease and 84 patients with LBD (68 dementia with Lewy bodies and 16 Parkinson's disease dementia).ResultsWe found that 80% had stable NPI total ≥1, 50% had stable modest NPI total ≥12 and 25% had stable NPI total ≥24 scores. Very severe NPS (≥48) were mostly single episodes, but 8% of patients with Alzheimer's disease had stable severe NPS. Patients with Alzheimer's disease and the highest 20% NPI total scores had a more stable or relapsing course of four key symptoms: aberrant motor behaviour, aggression/agitation, delusions and irritability (odds ratio 55, P < 0.001). This was not seen in LBD. Finally, 57% of patients with Alzheimer's disease and 84% of patients with LBD had reoccurring psychotic symptoms.ConclusionsWe observed a highly individual course of NPS, with most presenting as a single episode or relapsing; a stable course was less common, especially in LBD. These findings demonstrate the importance of an individualised approach (i.e. personalised medicine) in dementia care.

scholarly journals Benzodiazepines and antidepressants: effects on cognitive and functional decline in Alzheimer’s disease and Lewy body dementia

2020 ◽  
Author(s):  
Miguel Germán Borda ◽  
Alberto Jaramillo‐Jimenez ◽  
Ragnhild Oesterhus ◽  
Jose Manuel Santacruz ◽  
Diego Alejandro Tovar‐Rios ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Functional Decline ◽  
Lewy Body Dementia
Sign in / Sign up

Export Citation Format

Share Document