Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0752347 (Dementia with Lewy bodies)
 1,653 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical signs and symptoms preceding the onset of dementia are sometimes acute, such as mood disorders often associated with hypochondriacal traits and cognitive slowing, sudden and serious suicide attempts, character and conduct disorders contrasting with the previous state, and psychotic disorders presenting as pathological mistrust, or ill-structured prejudice or persecution. Most forerunning symptoms reflect a progressive deterioration of cognitive functions over a long period, that have been masked by various coping strategies used by the patient with the spouse's help. Progressive cognitive deficits may develop over years before dementia can be diagnosed with confidence. Quantitative tools can help to detect dementia incipiens, such as the Folstein Mini Mental Test, the Mattis Dementia Scale, the five-word learning test, the clock drawing test, and the brief cognitive battery. The profile of early cognitive deterioration varies according to the type of dementia (Alzheimer's disease, fronto-temporal dementia, Lewy body dementia, and vascular dementia). The symptoms of dementia may be interlinked with symptoms of other disorders. Neuropsychological tests and brain imaging are needed to validate the diagnosis.
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PMID:[Early clinical signs of dementia in the elderly]. 1666 38

Behavioral symptoms start to appear in mild and moderate dementia and become increasingly severe with the progression of the disease. Agitation, aggressiveness, and psychosis can be seen in Alzheimer's disease, and in particular are common manifestations in Lewy body dementia. It is the behavioral disturbances rather than the cognitive disorders that are more often the cause of the institutionalization of these patients because of the heavy assistance and emotional burden they represent for caregivers. Traditionally, these kinds of symptoms were controlled by classical antipsychotic agents, which after long-term use cause severe extrapyramidal effects, late dyskinesia, sedation, orthostatic hypotension, and cognitive function impairment. More recently, atypical antipsychotic agents have shown a better tolerability profile, with a reduced incidence of extrapyramidal effects, orthostatic hypotension, sedation, and a reduced impact on cognitive function. The aim of this study is to evaluate the efficacy and tolerability of quetiapine in a group of patients with a diagnosis of dementia and concomitant psychotic disorders. The response to treatment was evaluated by the Neuropsychiatric Inventory (NPI) and the Behavioral Pathology in Alzheimer's Disease Rating Scale (BEHAVE-AD). The NPI and BEHAVE-AD were administered at baseline and after 4 weeks and 12 weeks of therapy. Tolerability was assessed by the incidence of clinically evident side effects. The results show that quetiapine is effective in reducing behavioral symptoms, deliria and hallucinations, aggressiveness, and sleep disturbances. Quetiapine tolerability proved to be satisfactory. The only side effect of clinical significance was orthostatic hypotension, which was, however, partially preventable by a slower drug titration.
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PMID:Efficacy and tolerability of quetiapine in the treatment of behavioral and psychological symptoms of dementia. 1726 78

Clinical criteria for DLB have been more and more accurate over time, and they had focused on psychotic symptoms for their high frequency. Recent literature suggests that behavioral and psychological symptoms of dementia (BPSD) are frequently associated with DLB, beyond the presence of psychosis. Notwithstanding, the occurrence of BPSD in DLB is under-investigated, and no data are available yet in the different stages. Aim of the present study was to evaluate BPSD pattern in the different stages of DLB, and characterize the relationship with both cognitive deficits and Parkinsonian signs. Ninety-two DLB patients were enrolled and were divided into mild (n=63, 68.5%) and moderate-severe (n=29, 31.5%) subgroups according to the severity of cognitive impairment. Considering the absence/presence of symptoms, anxiety was the most common BPSD (67.4%), followed by depression (61.9%), apathy (57.6%), agitation and sleep disorder (55.4%). Psychosis was present in half of the patients. These symptoms worsened over disease course and represented a core-feature of the disease. No association between BPSD severity and the degree of motor disability was found. These observations suggest that a careful and systematic evaluation of BPSD is mandatory for carefully characterizing disease-related features and for developing new therapeutic approaches. Knowledge of the specific weight of BPSD in DLB would contribute to improve the allocation of health resources for dementia and to a better management of the disease.
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PMID:Behavioral and psychological symptoms in dementia with Lewy-bodies (DLB): frequency and relationship with disease severity and motor impairment. 1746 82

Dementia with Lewy Bodies (DLB) is the second most common form of dementia in the elderly. Core features of the DLB are fluctuating cognitive symptoms, visual hallucinations and spontaneous parkinsonism. The clinical diagnostic criteria are very useful in the differentiation between DLB and Alzheimer's disease. The deficits in cholinergic neurotransmission are pronounced and associated with cognitive and psychotic symptoms. An 83 years old patient with DLB showed well formed recurrent visual hallucinations and fluctuating cognition and attention. There was no response to treatment with atypical neuroleptics. The patient responded within few days to treatment with Donepezil. Both cognitive and behavioural symptoms were improved significantly.
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PMID:[Dementia with Lewy bodies. Clinical improvement under treatment with an acetylcholinesterase inhibitor]. 1749 20

Dementia with Lewy bodies (DLB) is a progressive dementia frequently accompanied by psychotic symptoms. Similar symptoms can occur in Alzheimer's disease (AD) to a lesser extent. The use of neuroleptic medication to treat psychosis in both diseases is of modest efficacy and can induce severe adverse reactions in DLB. Dopamine D2 receptors in the cerebral cortex are the putative target for the antipsychotic action of these drugs, but the status of these receptors in DLB is unknown. Autoradiography was used to examine the density D2 receptors in postmortem temporal cortex tissue from prospectively assessed patients with neuropathologically confirmed DLB and AD. D2 receptors were substantially (over 40%) and significantly (P < 0.001) reduced in temporal cortex in DLB, and in DLB with concomitant Alzheimer pathology, but was not significantly changed in AD. This reduction correlated with greater cognitive decline (P < 0.01), but was not significantly related to visual or auditory hallucinations or delusions. D2 receptor density was inversely correlated with cortical Lewy body pathology in the neocortex (P < 0.001). The specific loss of D2 receptors associated with Lewy body pathology, in conjunction with our previous finding of low D2 receptors in striatum in DLB, provides a possible explanation for neuroleptic intolerance. That the reduction of D2 receptors correlated with cognitive decline suggests that neuroleptics, as dopamine D2 receptor antagonists, may have a deleterious effect on cognition in DLB.
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PMID:Selective loss of dopamine D2 receptors in temporal cortex in dementia with Lewy bodies, association with cognitive decline. 1766 55

Dementia with Lewy bodies (DLB) is a progressive disease of the nervous system manifested with dementia, parkinsonism, psychotic and autonomic disturbances. To estimate efficacy and safety of memantine in patients with clinically diagnosed DLB (according to criteria of McKeith et al., 1999), an open controlled 16-week trial was carried out in 23 patients, mean age 69,2+/-5,9 years. Patients were divided into 2 groups: 14 patients who received memantine in dosage 20 mg/d and 9 patients of a control group. A battery of neuropsychological tests, clinical assessment using fluctuation scales, scales for assessment of behavioral and psychotic disturbances, the General Clinical Impression scale were used. Memantine significantly improved cognitive dysfunction throughout the study (the mean MMSE scorer were increased by 1,5 points compared to the baseline) especially due to the improvement of attention and executive functions. The reduction of fluctuations of mental status, aggressiveness, aspontaneity, disinhibition was also observed. There were no significant changes of Parkinsonian and psychotic symptoms severity. Good tolerability of memantine is noted: only 2 patients were withdrawn from the study because of episodes of confusion on the titration phase of the trial.
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PMID:[Efficacy and safety of memantine in dementia with Lewy bodies]. 1857 56

Dementia with Lewy bodies (DLB), the second most frequent cause of dementia after Alzheimer disease (AD), is characterized by the widespread distribution of Lewy bodies in virtually every brain area. Clinically, DLB is distinguished from AD by fluctuating cognition, prominent visual hallucinations and parkinsonism, and from Parkinson disease, by the appearance of parkinsonism within one year of cognitive or behavioral decline. The main component of Lewy bodies is alpha-synuclein. Accumulating evidence suggests that its aggregation constitutes one of the first steps preceding Lewy body formation, so that antiaggregation strategies would be very useful to prevent alpha-synuclein fibril formation. Main therapies nevertheless applied up to the present remain symptomatological. In this context, cholinesterase inhibitors such as rivastigmine, galantamine and donepezil, are used for the treatment of delusions and other psychotic symptoms. This review focuses on the recent discovery of possible alpha-synuclein anti-aggregation factors, where four main classes can be defined. First, beta-synuclein as well as alpha-synuclein derived peptides in addition to antibodies present a group of proteins and peptides that directly interact with alpha-synuclein and so inhibit its aggregation. Second, small molecules interfere with alpha-synuclein aggregation by their covalent binding, although not all of them are suitable for an appropriate inhibition of alpha-synuclein aggregation. Third, to inhibit the expression of alpha-synuclein and its isoforms at the RNA level, the use of interference RNA represents a future challenge. The fourth strategy is based on the enhancement of inclusion body formation to accelerate the elimination of soluble alpha-synuclein oligomers. Each chapter section includes the discussion of possible strategies for the development of drugs and therapies.
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PMID:The therapeutical potential of alpha-synuclein antiaggregatory agents for dementia with Lewy bodies. 1899 34

The objective of this study is to evaluate psychiatric symptoms in Parkinson's disease (PD) patients and to assess their relation with other clinical aspects of PD. Psychotic symptoms (PS) and compulsive symptoms (CS) as well as other nonmotor and motor features were evaluated in 353 PD patients. Psychotic and compulsive symptom scores did not correlate significantly. PS occurred in 65% of patients, with item frequencies ranging from 10% (paranoid ideation) to 55% (altered dream phenomena). Regression analysis showed that autonomic impairment accounted for 20% of the 32% explained variance of PS, whereas cognitive problems, depression, daytime sleepiness, and dopamine agonist (DA) dose explained the rest. CS occurred in 19%, with item frequencies of 10% for both sexual preoccupation and compulsive shopping/gambling. Patients with more severe CS (score > or = 2 on one or both items) were significantly more often men, had a younger age at onset, a higher DA dose and experienced more motor fluctuations compared to the other patients. PS and CS are common but unrelated psychiatric symptoms in PD. The relations found between PS and cognitive problems, depression, daytime sleepiness, and autonomic impairment suggests a resemblance with Dementia with Lewy Bodies. The prominent association between PS and autonomic impairment may be explained by a shared underlying mechanism. Our results confirm previous reports on the profile of patients developing CS, and mechanisms underlying motor fluctuations may also play a role in the development of CS in PD.
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PMID:Psychotic and compulsive symptoms in Parkinson's disease. 1913 65

Lewy body dementia (LBD) is a progressive brain disease manifest as dementia and parkinsonism, along with psychotic and autonomic disorders. Although studies in recent years have demonstrated the positive effects of cholinesterase inhibitors in LBD, the search for therapeutic agents with other mechanisms of action remains relevant. An open, controlled, 16-week study was performed with the aim of evaluating the efficacy and safety of memantine in patients with clinically diagnosed LBD (criteria of McKeith et al., 1999). The study included 23 patients (mean age 69.2 +/- 5.9 years), who were divided into two groups: 14 patients received memantine at a dose of 20 mg/day and nine patients constituted the control group. Efficacy was evaluated using a battery of quantitative neurospychological tests, clinical scales for assessment of fluctuations in mental states, scales for assessment of behavioral and psychotic disorders, and the general clinical impression scale. The results demonstrated that memantine had positive effects on the patients' general status and cognitive functions (increases on the mini mental state examination by 1.5 points), mainly because of improvements in attention and control functions. There were also reductions in the severity of fluctuations in mental state, aggressivity, lack of spontaneity, and disinhibition. The severity of psychotic and motor disorders did not change significantly. Tolerance of the agent was good, only two patients withdrawing from the study because of episodes of confusion during the dose titration period.
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PMID:Efficacy and safety of memantine in Lewy body dementia. 1951 47

Although Parkinson's disease (PD) is considered mainly a movement disorder, robust information accumulated during the last 30 years has shown that about 30% of PD patients may also suffer from psychosis, which deeply affects their quality of life and eventually brings them to permanent hospitalization in nursing homes. PD psychosis (PDPsy) mainly occurs after 10 or more years of treatment. The main features of PDPsy include recurrent and continuous hallucinations and delusions for at least 1 month. In addition, a recent consensus of the National Institute of Neurological Disorders and Stroke and National Institute of Mental Health Working Group also included illusions and a false sense of presence as "minor symptoms" supporting the diagnosis. In addition, accumulated clinical data have shown that "minor symptoms" and benign hallucinations also imply a bad prognosis with time. In the diagnostic criteria for PDPsy, it is considered that patients suffer from PD for at least more than 1 year before psychosis develops. If this is not the case, there is an unsolved problem of an overlapping diagnosis with Dementia with Lewy Bodies. Most clinicians consider that the main cause of psychosis is chronic exposure to dopaminergic medication. However, from an operational point of view there remain difficulties in defining a specific time of exposure and dose of treatment and the occurrence of PDPsy. Specific rating scales have been developed for the evaluation of PDPsy, such as the Parkinson Psychosis Rating Scale. The Scale for the Assessment of Positive Symptoms usually applied in schizophrenic patients has also proved useful for scoring psychotic symptomatology in PD. Clozapine in low doses has been proven to be the most effective antipsychotic medication for PDPsy. However, its use may cause neutropenia. Therefore, new atypical antipsychotic drugs with serotonin 5-HT2A receptor inverse agonist properties have been developed. Recently, pimavanserin--a 5-HT2A inverse agonist--has been studied. We hope that soon we will have the possibility to include new agents for the management of PDPsy.
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PMID:Hallucinations and psychosis in Parkinson's disease. 2012 47


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