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PubMed1999

The differentiation of semantic dementia and frontal lobe dementia (temporal and frontal variants of frontotemporal dementia) from early Alzheimer's disease: a comparative neuropsychological study.

The authors compared age-matched groups of patients with the frontal and temporal lobe variants of frontotemporal dementia (FTD; dementia of frontal type [DFT] and semantic dementia), early Alzheimer's disease (AD), and normal controls (n = 9 per group) on a comprehensive neuropsychological battery. A distinct profile emerged for each group: Those with AD showed a severe deficit in episodic memory with more subtle, but significant, impairments in semantic memory and visuospatial skills; patients with semantic dementia showed the previously documented picture of isolated, but profound, semantic memory breakdown with anomia and surface dyslexia but were indistinguishable from the AD group on a test of story recall; and the DFT group were the least impaired and showed mild deficits in episodic memory and verbal fluency but normal semantic memory. The frontal and temporal presentations of FTD are clearly separable from each other and from early AD.

Age Factors↗
PubMed2006

Family history of dementia: dementia with lewy bodies and dementia in Parkinson's disease.

Parkinson's disease with dementia (PD-D) and dementia with Lewy bodies (DLB) may result from the same neurodegenerative process with different temporal and spatial courses. The authors report an association between DLB and family history of dementia in a comparison study between patients with a clinicopathological diagnosis of PD-D and DLB. Findings suggest that positive family history for dementia is associated with DLB with a yet unknown mechanism.

Aged↗
PubMedDate not supplied

[Depression and dementia: contribution to the French validation of 2 depression scales: the Cornell Scale for Depression in Dementia and the Dementia Mood Assessment Scale].

This study establishes, in a sample of elderly demented patients, the validity of a french translation of two depression rating scales: Cornell Scale for Depression in Dementia (CSDD, Alexopoulos 1988), Dementia Mood Assessment Scale (DMAS, Sunderland 1988). Cognitive performances of 24 patients (mean age 77.9 +/- 7.4, 7 men 17 women), meeting DSM III-R criteria for dementia, have been evaluated. Four clinicians, blind to the clinical diagnosis of depression established by a psychogeriatrist, have evaluated the sample with the two scales. All patients present middle to severe dementia: MMS = 16.8 +/- 3.45. Eleven patients (45%) present moreover depression. Concurrent validity has been established against Hamilton Depression Rating Scale, test retest reliability, inter-rater reliability and internal consistency are established for each scale. These characteristics are pleading for a good reliability of the french translation of CSDD and DMAS, in the presence of cognitive impairment.

Aged↗
PubMed1991

SIDAM--A structured interview for the diagnosis of dementia of the Alzheimer type, multi-infarct dementia and dementias of other aetiology according to ICD-10 and DSM-III-R.

The SIDAM--a new instrument for the symptomatic diagnosis and measurement of dementia according to DSM-III-R and ICD-10--is described. It comprises a brief structured clinical interview, a range of cognitive tests (e.g. including the Mini-Mental State (Folstein et al. 1975)) which constitute a short neuropsychological battery and a section for clinical judgement and third party information. All items rely on DSM-III-R and ICD-10 algorithms. The SIDAM has a high overall test-retest reliability which equally holds true on the diagnostic, criterion and item level. It is a brief (average of 28 min), practical and easily scored diagnostic instrument, which reliably separates subjects with DSM-III-R and ICD-10 dementia from those without such a disorder. Good congruence was found between SIDAM diagnoses and corresponding ICD-9 expert diagnoses. Furthermore, the SIDAM-Score (SISCO) allows a detailed measurement of even low levels of cognitive impairment and provides quantification of severity grading of cognitive dysfunction.

Aged↗
PubMed2001

Haloperidol for agitation in dementia.

BACKGROUND: Agitation includes wandering, crying out, abusive vocalization, and assaultive behavior and occurs in up to 70% of patients with dementia. Although the neuroleptic haloperidol has been used for decades to control disruptive behavior in psychotic and demented patients, the effectiveness of this drug for agitated dementia remains in question. The first meta-analysis on the effectiveness of haloperidol for agitated dementia, published in 1990, was limited in scope and was unable to provide clear guidelines for the use of haloperidol for demented patients who are agitated. Meta-analyses in 1998 and 2000 examined haloperidol compared with other neuroleptics as well as with placebo and omitted a number of databases, including non-English language publications. To determine the effect of haloperidol, compared with placebo, in the control of agitated dementia and to make recommendations for future research in this area a more widely based, yet more highly focussed review was carried out. OBJECTIVES: The main objective was to determine whether evidence supports the use of haloperidol to treat agitation in demented patients. SEARCH STRATEGY: The CDCIG Specialized Register was searched to identify all available reports on haloperidol treatment of agitated dementia. SELECTION CRITERIA: We examined randomized, placebo-controlled trials, with concealed allocation, where subjects' dementia and agitation were assessed. Trials involving treatment of less than one week were not included. DATA COLLECTION AND ANALYSIS: 1. Two reviewers extracted data from included trials. 2. Data were pooled, where possible, and analysed using appropriate statistical methods. 3. Odds ratios or average differences were calculated. 4. Only 'intention to treat' data were included. Where a cross-over design was employed (Devanand, 1998), only the initial phase of the study was used to compare haloperidol versus placebo. 5. Sensitivity analysis was applied to heterogeneity of results and to gauge the effect of the included studies of small sample size. 6. In addition to the overall meta-analysis, individual analyses of the reports were carried out to examine the effect of degree of dementia, dose of haloperidol, and duration of therapy on agitated dementia. Analysis included the following groups: All patients treated with haloperidol compared with placebo. MAIN RESULTS: There were five included trials. All studies stated "intention to treat" analysis of their results. Three studies were from the United States, and two studies were from Europe. Two studies examined patients with various forms of dementia, and three studies included only patients with diagnosed Alzheimer's dementia. 1. Overall meta-analysis of the response of agitated patients to haloperidol, compared with controls, showed no improvement in agitation. There is some evidence that haloperidol helps to control aggression. Adverse reactions and dropouts were more frequent among haloperidol treated patients, compared with controls. This meta-analysis provided no information about the relationship between the degree of dementia, the kind of agitation manifested, or the dosage and duration of therapy with haloperidol and response to treatment of demented patients with agitation. 2. The results of this meta-analysis were too broad to permit specific recommendations for treatment of agitated dementia with haloperidol. 3. Higher dose haloperidol, or prolonged haloperidol (12 weeks compared with 3 - 6 weeks) was associated with increased side effects, largely related to Parkinsonian symptoms of rigidity and bradykinesia. REVIEWER'S CONCLUSIONS: 1. Haloperidol appeared to provide no improvement in agitation among demented patients compared with placebo, but side effects were frequent. 2. Dropout rates were higher for haloperidol compared with placebo treated patients, suggesting that side effects led to discontinuation of treatment in some patients. 3. Because of the wide focus of this meta-analysis, not enough information was provided to permit recommendations linking haloperidol treatment of agitated dementia to degree of dementia, manifestations of agitation, or dosage and duration of treatment of haloperidol. 4. Individual analysis of reports indicated that higher dose haloperidol (more than 2 mg per day) may have been more effective than lower dose haloperidol (less than 2 mg per day) in controlling aggression, but not other manifestations of agitation, among patients with mild to moderate dementia. 5. Similar analysis suggested that prolonged therapy with haloperidol (more than 3 - 6 wks) or higher dosage (more than 2 mg per day) was more likely to result in side effects than were short term therapy (3 weeks) or lower dose haloperidol (less than 2 mg per day). 6. The reports provided too little information to permit interpretation of the effect of degree or type of dementia on response to haloperidol. Except for a favorable response of aggression to haloperidol, no other manifestations of agitated dementia were found to have improved following therapy with haloperidol, compared with controls.

Aggression↗
PubMed2000

Piracetam for dementia or cognitive impairment.

OBJECTIVES: To determine the clinical efficacy of piracetam for the features of dementia or cognitive impairment, classified according to the major subtypes of dementia: vascular, Alzheimer's disease or mixed vascular and Alzheimer's disease or unclassified dementia or cognitive impairment not fulfilling the criteria for dementia. SEARCH STRATEGY: The Cochrane Dementia and Cognitive Impairment Group Register of Clinical Trials was searched using the terms "piracetam", "nootropic" and "2-oxo-l-pyrrolidine acetamide". Electronic bibliographic databases including Medline, Embase, PychLit, Current Contents, Sociofile were searched back to 1966 with the terms piracetam, nootropics, 2-oxo-1-pyrrolidine and trials. In addition the pharmaceutical company responsible for marketing most of the piracetam worldwide, UCB Pharma, provided a comprehensive list of abstracts, which included many unpublished studies. As many of these unpublished, placebo control studies will be reviewed as possible. SELECTION CRITERIA: All unconfounded trials specified as randomised in which treatment with piracetam was administered for more than a day and compared with placebo in patients with dementia of the Alzheimer's type, vascular dementia or mixed vascular and Alzheimer's disease or uncalssified dementia or cognitive impairment not fulfilling the criteria for dementia. DATA COLLECTION AND ANALYSIS: Data were extracted independently by two reviewers. Each study was independently verified as fulfilling the inclusion criteria. Studies were rated for methodological quality by assessment of blinding and loss before analysis as described by Jadad et al. (1996). Studies were pooled if appropriate and possible, and the pooled odds ratios (95%CI) or the average differences (95%CI) were estimated. Where possible, intention-to-treat data were used. Sensitivity analyses were performed to determine if successive elimination of those studies performing most poorly on these quality criteria changed the effect estimate. MAIN RESULTS: Unfortunately, many of these studies were crossover in design and data were unavailable from the first period. In many other studies data were not able to be extracted from the first period. From the data that were pooled there was only one outcome where significant amounts of evidence were available, Global Impression of Change. There was evidence of heterogeneity in the results from the individual studies, Chi squared test = 20.8 (df=5). Using a fixed effects model the odds ratio for improvement in the Piracetem group compared with the Placebo group was 3.55, [95% CI][2.45, 5.16]. If a random effects model was used the odds ratio was 3.47 [1.29, 9.30]. If one single-blind study was excluded, the fixed effects model yielded an odds ratio of 3.36 [2.29, 4.99] and if a random effects model was applied then the odds ratio was 2.89 [1.01, 8.24]. The evidence of effects on cognition and other measures, was inconclusive. REVIEWER'S CONCLUSIONS: At this stage the evidence available from the published literature does not support the use of Piracetem in the treatment of people with dementia or cognitive impairment because effects were found only on global impression of change but not on any of the more specific measures. There is a need for further evaluation of piracetam by : 1) Obtaining the data from these studies for an individual patient database review, 2) Performing a randomised trial of Piracetam in patients with diagnoses made by currently accepted diagnostic criteria. Piracetam should be trialled for a period of at least 6 months and preferably longer. Specific cognitive instruments which are sensitive to change, Clinician Global Impression of Change, levels of dependency and caregiver quality of life scales should also be incorporated in such a study.

Alzheimer Disease↗
PubMed1994

[Progress in vascular dementia--an overview of vascular dementia from past to new concepts].

This article summarizes various concepts (Binswangers encephalopathy, multiinfarct-dementia, lacunar state, mixed dementia, dementia due to amyloid angiopathy or vasculitis) and classifications (DSM, ICD, ADDTC) on vascular dementia. It reviews historical, clinical, and diagnostic aspects (i.e. neuroradiology, SPECT, PET) as well as therapeutic approaches. The confusing nomenclature on vascular dementia is discussed, considering especially the non-convincing concept of multiinfarct-dementia that often has been misused as a synonym for vascular dementia. Multiinfarct-dementia is now restricted to a syndrome of vascular dementia due to several large vessels strokes. A current definition and classification of vascular dementia as suggested by NINDS-AIREN international workshop is described. It defines criteria consistent with the diagnosis of "possible", "probable" and "definite" vascular dementia based on clinical, radiologic and neuropathologic features. The criteria of "probable" vascular dementia include all the following: 1. the presence of dementia and cerebrovascular disease defined by focal signs on neurologic investigation and evidence of relevant cerebrovascular disease by brain imaging (multiple lacunae, extensive white matter lesions, multiple large-vessels infarcts or a strategically placed infarct) 2. A relationship between dementia and cerebrovascular disease (onset of dementia within 3 months following a recognized stroke; abrupt deterioration, stepwise progression). This classification of vascular dementia emphasises pathogenetic aspects and includes dementia resulting from small- and large-vessels disease as well as hypoperfusion, haemorrhagic dementia and dementia due to still unknown factors. Operational criteria for the frequent Binswangers encephalopathy--a prototype of vascular dementia--are presented. Thereby a basis for further research and discussion in this exciting area should have been formed.

Dementia, Multi-Infarct↗
PubMed1997

Depressive dementia: a "transitional dementia"?

This review comprises a historical, clinical, and empirical examination of the dementia spectrum of depression. The primary focus of the article is to evaluate the usual dichotomy between depressive dementia as functional-reversible and degenerative dementia as organic-irreversible. It is proposed that depression, cognitive impairment, and degenerative dementia be viewed as intersecting continua. Five prototypical groups are defined along these continua: (1) major depression without depressive dementia, (2) depressive dementia, (3) degenerative dementia without depression, (4) depression of degenerative dementia, and (5) random co-occurrence of depression and degenerative dementia. The data suggest that a subset of cases of major depression without dementia appear to evolve into depressive dementia, and in turn, depressive dementia may constitute a risk factor for degenerative dementia. Depressive dementia and degenerative dementia can sometimes represent two different points of organic deterioration and severity in a long-term, multiphasic disease course; depressive dementia sometimes appears to be a transitional stage or phase in a disease progression from depression without dementia to a degenerative dementia. The concept of "transitional dementia" is introduced in a heuristic and preliminary attempt to accommodate the nosologic entity of depressive dementia.

Aged↗
PubMed2003

Memantine for dementia.

BACKGROUND: Alzheimer's disease, vascular and mixed dementia are the commonest forms of dementia in older people. There is evidence that the excitatory activity of L-glutamate plays a role in the pathogenesis of Alzheimer's disease and in the damage from an ischaemic stroke. A low affinity antagonist to N-Methyl-D-aspartate (NMDA) type receptors, such as memantine, may prevent excitatory amino acid neurotoxicity without interfering with the physiological actions of glutamate required for memory and learning. OBJECTIVES: To determine the clinical efficacy and safety of memantine for people with Alzheimer's disease, vascular, or mixed dementia. SEARCH STRATEGY: Trials were identified from a search of the Trial-based Specialized Register of the Cochrane Dementia and Cognitive Improvement Group on 9 October 2002 using the terms: memantin*, D-145, DMAA, DRG-0267. All major health care databases and trial databases within the scope of the group are searched regularly to keep this Register up to date. SELECTION CRITERIA: Double-blind, parallel group, placebo-controlled, randomized and unconfounded trials in which memantine was administered to people with dementia. DATA COLLECTION AND ANALYSIS: Data were extracted, pooled where possible, and weighted mean differences, standardized mean differences or odds ratios were estimated. Intention-to-treat (ITT) and observed cases (OC) analyses are reported, where data were available. MAIN RESULTS: There were a total of seven trials that met inclusion criteria, of which five had sufficient data for analysis. The analysis of change from baseline for cognition gave statistically significant results in favour of memantine (20 mg/day) (MD: -2,83 95% CI -4.37 to -1.29, P=0.0003) at 28 weeks and for memantine (30mg/day) at 6 weeks (MD: -3.04. 95% CI -5.68 to -0.40, P=0.02). Effects on Activities of Daily living (ADL) were difficult to interpret. One study provided data using a non-validated scale for measuring five simple instrumental tasks under the guidance of an investigator. When pooled with another study the analysis gave statistically significant results in favour of memantine for 30 mg/day at 6 weeks (SMD: -1.36 95% CI -1.77 to -0.96, P=0.0003). Mood and behaviour: One trial provided data on memantine 30 mg/day at 6 weeks using the NOSIE scale. The OC analysis found statistically significant differences in favour of treatment (MD: 23.30 95% CI 17.83 to 28.77, P<0.00001). Global scales: The analysis revealed a statistically significant difference in favour of memantine (20mg/day ) at 6 weeks (MD: -12.30 95% CI -16.90 to -7.70, P<0.00001). Similar results were found for larger doses (memantine 30 mg/day) at 6 weeks in a pooled meta-analysis of two other studies (WMD: -10.77 95% CI -13.46 to -8.09, P<0.00001). With regard to the Global Impression of Change three studies found statistically significant results in favour of 10, 20 and 30 mg/day of memantine compared with placebo at 6 or 12 weeks. There was a benefit in favour of memantine (20 mg/day) compared with placebo at 6 weeks, for the numbers improved ( 24/41 compared with 11/41)(OR, 3.85, 95% CI 1.52 to 9.75, P=0.004), in favour of memantine (30 mg/day) compared with placebo at 6 weeks, for the numbers improved ( 20/30 compared with 8/29)(OR, 5.25, 95% CI 1.72 to 15.98, P=0.004) and in favour of memantine (10 mg/day) compared with placebo at 12 weeks, for the numbers improved ( 60/82 compared with 38/84)(OR, 3.30, 95% CI 1.72 to 6.33, P=0.0003). In general memantine seemed to be well tolerated. There was no statistically significant difference between memantine and placebo for the three studies that reported adverse events. There were some data on specific adverse events. In one study the incidence of restlessness by the end of the treatment at 6 weeks was statistically significantly lower in the placebo group than in the group taking memantine 30 mg/day (15/30 compared with 2/29) (OR 13.50, 95% CI 2.71 to 67.19, P=0.001). The number of dropouts was similar in treatment and placebo groups at 6 or 28 weeks time for memantine 20 mg/day and at 6 weeks for memantine 30 mg/day. REVIEWER'S CONCLUSIONS: Memantine is a safe drug and may be useful for treating Alzheimer's, vascular,and mixed dementia of all severities. Most of the trials so far reported have been small and not long enough to detect clinically important benefits. However there is a possible benefit on cognition and global measures, and an early improvement in behaviour in people with dementia. More studies are needed.

Activities of Daily Living↗
PubMed2000

Music therapy for dementia symptoms.

BACKGROUND: While music/music therapy does not represent a treatment of dementia, its use is based on a possible beneficial effect on symptoms including social, emotional and cognitive skills and for decreasing behavioral problems of individuals with dementias. Thus, there are clear implications for patients' and caregivers' quality of life. However, quantification and documentation of the evidence of this effect is necessary. Professional music therapists are accountable for providing efficient, beneficial treatment. Further, music therapists are responsible for assessing, designing and implementing music therapy treatments, monitoring client progress, and reformulating their practice according to data collected and new advancements in the field. If they wait until sufficient valid, empirical data on all aspects of a disability or music response are available before attempting to design a therapy session, they may well reach retirement age before even one client can be served. On the other hand, promulgating the efficacy of music therapy in general, or of specific music therapy techniques, in the absence of any substantiation other than intuition or tradition borders on professional recklessness. OBJECTIVES: To gather and evaluate the evidence for the effectiveness of music therapy for dementia symptoms. SEARCH STRATEGY: All available sources of references were searched for randomised controlled trials of music therapy used as an intervention in dementia. The search terms included 'controlled trial or study, music*, therapy, dement*, Alzheimer*, cognitive impairment.' SELECTION CRITERIA: The reviewers assessed the methodological quality of the studies available for inclusion. The criteria used are presence and adequacy of a control condition, independent assessment of patients' performance (ie standardized ratings carried out by a person other than the music therapist) and the number of participants (no fewer than three). DATA COLLECTION AND ANALYSIS: No randomised controlled trials, or trials with quantitative data suitable for analysis were found. MAIN RESULTS: The research into music therapy to date has lacked methodological design rigour. However, the research evidence available provides sufficient grounds on which to justify further investigations into the use of music therapy in dementia patients. In this context, the reviewers discuss some of the issues and research from the studies that were considered for inclusion. REVIEWER'S CONCLUSIONS: This review was not able to identify reliable empirical evidence on which to justify the use of music therapy as a treatment for dementia. However, the evidence available suggests that music therapy may be beneficial in treating or managing dementia symptoms, and the predominant conclusion of this review is the highlighting of the need for better designed studies of the intervention.

Alzheimer Disease↗
PubMed2000

Validation therapy for dementia.

BACKGROUND: Validation therapy is a "therapy for communicating with old-old people who are diagnosed as having Alzheimer's disease and related dementia". The approach was developed by Naomi Feil between 1963 and 1980. She classifies individuals with cognitive impairment as having one of four stages on a continuum of dementia: these stages are Malorientation, Time Confusion, Repetitive Motion and Vegetation. The benefits of Validation therapy for patients are reported by Feil as restoration of self worth, minimisation of the the degree to which patients withdraw from the outside world, promotion of communication and interaction with other people, reduction of stress and anxiety, stimulation of dormant potential, help in resolving unfinished life tasks, facilitation of independent living for as long as possible. These benefits are highly desirable and Validation therapy but there is a need to show them on the basis of substantive research yielding strong evidence across a number of well designed studies. The potential number of people that might benefit from the implementation of Validation therapy is considerable given the increasing incidence of dementia. OBJECTIVES: To evaluate the effectiveness of using validation therapy with people diagnosed as having senile dementia of the Alzheimer's type, other forms of dementia, or cognitive impairment. SEARCH STRATEGY: The Cochrane Controlled Trials Register was searched by the Cochrane Dementia and Cognitive Impairment Group Coordinator and relevant references were forwarded to the primary reviewer. The reviewers carried out independent searches of the following electronic databases - MEDLINE, EMBASE, Eureka, CINAHL, PSYCLIT, RLIN, SIGLE and SOCIOFILE. The following key terms were used in searches; validation-therapy, dementia, cognitive impairmnent, communication, and random*-control*. An author search using Feil and Naomi was also carried out. Personal contact was made with the Validation Institute, Cleveland, Ohio USA and unpublished studies were sought by direct contact with the relevant authors, or institutions. Key individuals who might provide further information regarding validation therapy were contacted. SELECTION CRITERIA: All randomised controlled trials (RCTs) and quasi-randomised controlled trials examining Validation therapy as an intervention for dementia were considered for inclusion in review. The criteria for inclusion/exclusion comprised systematic assessment of the quality of study design and the risk of bias, using a standard data extraction form. Outcome measures of cognitive and/or behavioural change were required. DATA COLLECTION AND ANALYSIS: Data were extracted independently by both reviewers, using a previously tested data extraction form. Authors were contacted for data not provided in the papers. Psychological scales measuring cognitive and behavioural changes were examined. Subcategory analysis was performed due to the diversity of the scales and the inability to combine data across studies. MAIN RESULTS: Only three studies were identifed that potentially met the inclusion criteria and only two small studies were able to be obtained. The Peoples 1982 study was not obtainable through a British Library loan because the cost was prohibitive. Data from 2 studies were entered using MetaView - Robb 1986, Toseland et al 1997, incorporating data on a total of 87 patients (32 in the experimental group, and 55 in the control groups (usual care 34 and social contact 21)). It was not possible to pool the data from the two included studies, and therefore, subcategory analyses were carried out. The analysis of the data failed to reveal statistically significant results although there were trends toward favouring validation therapy for some outcomes. (ABSTRACT TRUNCATED)

Alzheimer Disease↗
PubMed2003

Distinctive neuropsychological patterns in frontotemporal dementia, semantic dementia, and Alzheimer disease.

OBJECTIVE: To assess the ability of a brief neuropsychological bedside screening battery to discriminate between Alzheimer disease, frontotemporal dementia, and semantic dementia. METHODS: Subjects were 21 patients with frontotemporal dementia, 14 patients with semantic dementia, and 30 patients with Alzheimer disease comparable in terms of Mini Mental Status Examination score, age, and education. Frontotemporal dementia and semantic dementia diagnoses were made clinically using the consensus criteria of Neary et al. 1 Subjects were administered a brief neuropsychological screening assessing episodic memory, working memory, executive function, naming, spatial ability, abstract reasoning, and calculations. RESULTS: Both the Alzheimer disease and semantic dementia groups were significantly impaired relative to the frontotemporal dementia group on verbal memory, whereas only the Alzheimer disease group was impaired on visual memory. Frontotemporal dementia patients performed significantly worse on backward digit span and made significantly more executive errors than Alzheimer disease and semantic dementia patients. Semantic dementia patients were more impaired than Alzheimer disease and frontotemporal dementia patients on confrontation naming. Discriminant function analyses identified the 5 most discriminating variables that correctly classified 89.2% of cases. CONCLUSIONS: Frontotemporal dementia, semantic dementia, and Alzheimer disease are associated with distinct neuropsychological profiles that classify these dementia syndromes with considerable success. The neuropsychological profiles highlight the distinctiveness between the 3 syndromes, are consistent with the known loci of neuropathology in these conditions, and can potentially serve as an adjunct to the current clinical criteria.

Aged↗
PubMed1996

A study of the characteristics of the dementia patients and caregivers in dementia-nonspecific adult day care programs.

OBJECTIVE: To determine if basic differences exist between the patients and caregivers of a representative group of dementia-nonspecific medical versus social adult day care centers with specific programs for dementia patients. DESIGN: A telephone interview questionnaire survey. SETTING: North Central North Carolina. PARTICIPANTS: A total of 242 adult day care dementia patients and caregivers from three medical and three social nondementia-specific adult day care centers. MEASUREMENTS: Dementia patient variables: Day care subtype (medical or social); length of stay; number of days attended; age; sex; race; educational level; marital status; religious affiliation; income; living status; number of medical conditions; number of prescription medications; function; ADL status (walking, eating, bathing, dressing, grooming, toileting); continence status; number and type of abnormal behaviors; formal help status (hospitalization during day care, part or full-time nursing home attendance, or home healthcare assistance); transportation; and financial assistance. Caregiver variables: day care subtype; age; sex; race; educational level; marital status; religious affiliation; income; number of medical conditions; number of prescription medications; informal help (family friends or other non-paid help); paid help (friend, other, home health, or nursing home); relationship to patient; employment status; and level of caregiver burden. MAIN RESULTS: There were 144 medical and 62 social adult day care dementia patients and caregivers who agreed to participate. The average age of the patient was 77.9 years (SD +/- 8.4), and that of the caregiver was 57.7 years (SD +/- 13.9); 68.4% of the patients and 75.4% of the caregivers were females. Dementia patients in the medical subtype day care had a shorter length of stay than social day care patients; this did not reach statistical significance. There were significantly more white patients and caregivers in the medical than in the social subtype day care, 83.1% versus 50% and 83.3% versus 50.8%, respectively. Dementia patients of the medical subtype also had significantly more education, income, less function, and more symptoms of depression than dementia patients in the social subtype. Dementia patients of the medical subtype also had more abnormal psychological behaviors than their social subtype counterparts, with borderline significance (P = .071). There were more married caregivers in the medical subtype than in the social subtype day care. Caregivers of dementia patients in the medical subtype had significantly more paid help and caregiver burden than did caregivers of dementia patients in the social subtype. CONCLUSIONS: In this study, there appear to be key differences between the dementia patients and caregivers of medical versus social adult day care centers as to demographic and health-related variables. The differences in demographic variables appear to be associated with socioeconomic factors, whereas the decreased function and greater number of depressive symptoms of the medical dementia patients may reflect poorer health as reflected by the greater amount of paid help and increased caregiver burden experienced by the caregivers of medical dementia patients. These findings should be verified in prospective studies.

Adult↗
PubMed2001

Distinct behavioural profiles in frontotemporal dementia and semantic dementia.

OBJECTIVE: To test predictions that frontotemporal dementia and semantic dementia give rise to distinct patterns of behavioural change. METHODS: An informant based semistructured behavioural interview, covering the domains of basic and social emotions, social and personal behaviour, sensory behaviour, eating and oral behaviour, repetitive behaviours, rituals, and compulsions, was administered to carers of 41 patients with semantic dementia and with apathetic (FTD-A) and disinhibited (FTD-D) forms of frontotemporal dementia. RESULTS: Consistent with prediction, emotional changes differentiated FTD from semantic dementia. Whereas lack of emotional response was pervasive in FTD, it was more selective in semantic dementia, affecting particularly the capacity to show fear. Social avoidance occurred more often in FTD and social seeking in semantic dementia. Patients with FTD showed reduced response to pain, whereas patients with semantic dementia more often showed exaggerated reactions to sensory stimuli. Gluttony and indiscriminate eating were characteristic of FTD, whereas patients with semantic dementia were more likely to exhibit food fads. Hyperorality, involving inedible objects, was unrelated to gluttony, indicating different underlying mechanisms. Repetitive behaviours were common in both FTD and semantic dementia, but had a more compulsive quality in semantic dementia. Behavioural differences were greater between semantic dementia and FTD-A than FTD-D. A logistic regression analysis indicated that emotional and repetitive, compulsive behaviours discriminated FTD from semantic dementia with 97% accuracy. CONCLUSION: The findings confirm predictions regarding behavioural differences in frontotemporal and semantic dementia and point to differential roles of the frontal and temporal lobes in affect, social functioning, eating, and compulsive behaviour.

Behavior↗
PubMed1999

White matter lesions on magnetic resonance imaging in dementia with Lewy bodies, Alzheimer's disease, vascular dementia, and normal aging.

OBJECTIVES: Alzheimer's disease and vascular dementia are associated with an increase in changes in white matter on MRI. The aims were to investigate whether white matter changes also occur in dementia with Lewy bodies and to examine the relation between white matter lesions and the cognitive and non-cognitive features of dementia with Lewy bodies, Alzheimer's disease, and vascular dementia. METHODS: Proton density and T2 weighted images were obtained on a 1.0 Tesla MRI scanner in patients with dementia with Lewy bodies (consensus criteria; n=27, mean age=75.9 years), Alzheimer's disease (NINCDS/ADRDA; n=28, mean age=77.4 years), vascular dementia (NINDS/AIREN; n=25, mean age=76.8 years), and normal controls (n=26, mean age=76.2 years). Cognitive function, depressive symptoms, and psychotic features were assessed using a standardised protocol. Periventricular hyperintensities (PVHs), white matter hyperintensities (WMHs) and basal ganglia hyperintensities (BGHs) were visually rated blind to diagnosis using a semiquantitative scale. RESULTS: Periventricular hyperintensities were positively correlated with age and were more severe in all dementia groups than controls. Total deep hyperintensities scores (WMHs plus BGHs) were significantly higher in all dementia groups than controls and higher in patients with vascular dementia than those with dementia with Lewy bodies or Alzheimer's disease. In all patients with dementia, frontal WMHs were associated with higher depression scores and occipital WMHs were associated with an absence of visual hallucinations and delusions. CONCLUSION: In common with Alzheimer's disease and vascular dementia, PVHs and WMHs were significantly more extensive in dementia with Lewy bodies than in controls. This overlap between different dementias may reflect shared pathological mechanisms. The link between frontal WMHs and depression and the absence of occipital WMHs and psychotic symptoms has important implications for understanding the neurobiological basis of these symptoms.

Aged↗
PubMed1997

Comparative evolution of Alzheimer disease, vascular dementia, and mixed dementia.

OBJECTIVE: To compare the evolution of Alzheimer disease (AD), vascular dementia (VaD), and mixed dementia by cognitive domain. SETTING: The University of Western Ontario Dementia Study, which is a registry of cases of dementia seen for secondary and tertiary assessment in a university memory disorders clinica with extensive follow-up data and histopathological confirmation of clinical diagnoses. PATIENTS: One hundred twenty-nine patients with definite or probable AD, 12 patients with definite or probable VaD, and 36 patients with definite or probable mixed dementia. METHODS: Patients were grouped as having an early, moderate, or advanced stage of disease according to the extended scale for dementia (ESD). The ESD was subdivided into cognitive domains, and the domain scores were compared for each stage of disease by diagnostic category with the use of a 2-way analysis of variance with repeated measures. RESULTS: As expected, the scores in all domains decreased significantly with increasing severity. There was a significant difference in the decline in memory among the diagnostic groups (P = .02) that was mostly attributable to the difference between AD and mixed dementia (P = .03), with the difference between AD and VaD only approaching significance (P = .06). There was a similar finding for praxis. The interaction between diagnosis (AD and VaD) and severity was significant only for memory (P = .02), showing a less severe memory deficit at onset but a proportionately more rapid progression in VaD and arithmetic ability (AD and mixed dementia [P = .03]). CONCLUSIONS: Alzheimer disease, VaD, and mixed dementia evolve similarly as assessed using cognitive domains obtained by subdivision of the ESD in a patient population derived from a memory clinic and by analyzing VaD as a single entity. Only memory impairment evolves differently between AD and VaD, with this depending on the severity. Memory is more severely impaired in the early stage of AD; however, with increasing severity of dementia, memory impairment in VaD accelerates and catches up with AD at the level of moderate impairment. The differences between AD and mixed dementia are greater than those between mixed dementia and VaD, suggesting an important role for the ischemic component of mixed dementia. Simple neuropsychological tools (eg, the ESD) may be incapable of distinguishing between AD and VaD, and more focused instruments may be required. Inherent bias in case selection may prevent extrapolation of these results to VaD in general, but the neuropsychological criteria for VaD may need to vary, depending on the severity.

Alzheimer Disease↗
PubMed2000

Aspirin for vascular dementia.

BACKGROUND: For patients with a diagnosis of vascular dementia there is evidence that aspirin is widely prescribed - in one study, completed by geriatricians and psychiatrists in the UK, 80% of patients with cognitive impairment (with vascular risk factors) were prescribed aspirin. However, a number of queries remain unanswered: Is there convincing evidence that aspirin benefits patients with vascular dementia? Does aspirin affect cognition or improve prognosis? In addition, does the risk of cerebral or gastric haemorrhage outweigh any benefit? The aim of this review is to assess the evidence of effectiveness of aspirin in those with a diagnosis of vascular dementia. OBJECTIVES: To assess the evidence of effectiveness of the use of aspirin for vascular dementia. SEARCH STRATEGY: Computerised databases were searched independently by two reviewers. In addition, relevant websites were searched and some journals were handsearched. Specialists in the field were approached for unpublished material and also any publications found were searched for additional references. SELECTION CRITERIA: All randomised controlled trials investigating the effect of aspirin for vascular dementia are included. Inclusion/exclusion of studies comprised systematic assessment of the quality of study design and the risk of bias. DATA COLLECTION AND ANALYSIS: Data were extracted independently by both reviewers, using a previously tested data extraction form and, where required, authors were contacted for data not provided in the papers. The aim was to evaluate data recorded via tools assessing cognitive and behavioural changes along with mortality, morbidity and institutionalisation data. MAIN RESULTS: One randomised controlled trial ( approximately approximately Meyer 1989 approximately approximately ) was included, and yielded data for analysis on a total of 70 patients. The only relevant outcome assessed in this trial was cognition. Change in cognitive outcome was towards being in favour of treatment. REVIEWER'S CONCLUSIONS: There is very limited evidence that aspirin is effective in treating patients with a diagnosis of vascular dementia. Further research is needed to assess the effect of aspirin on cognition, and also on additional outcomes such as behaviour, and quality of life. At present it is not possible to provide evidence for other queries regarding the use of aspirin for dementia (these are described in the Background section of this review).

Aspirin↗
PubMed1995

[Difference in MRI findings and risk factors between multiple infarction without dementia and multi-infarct dementia].

MRI findings and risk factors for vascular dementia were evaluated with multi-variate analysis in 96 multi-infarct patients without dementia and 40 multi-infarct patients with dementia (MID). Only subjects with small infarcts in the territory of the perforator artery or deep white matter were studied. The diagnosis of MID was diagnosed according to DMS-III criteria and Hachinski's ischemia score. Location and area of patchy high-intensity areas including small infarcts, the degree of periventricular high intensity (PVH), and the degree of brain atrophy were examined with MR images. Independent variables were: history of hypertension, diabetes mellitus, other complications; systolic and diastolic blood pressure, atherosclerotic index, hematocrit, history of smoking, level of education, and activities of daily life (ADL). Hayashi's quantification method II was used to analyze the data. The most significant correlation was found between history of hypertension and dementia (partial correlation coefficient: 0.39). Significant correlations were also found between ADL and dementia (0.32), between thalamic infarction and dementia (0.31), and between PVH and dementia (0.27). Age, brain atrophy index, and history of diabetes mellitus contributed little to dementia. The contribution to dementia did not differ significantly between right and left patchy high-intensity areas on MR images. Location of infarcts, except for bilateral thalamic infarcts and large PVH, contributed little to dementia. Thus it would be difficult to base a prediction of the prevalence of vascular dementia on MRI findings. However, both hypertension and ADL contribute to vascular dementia and both are treatable, which may be significant for the prevention of dementia.

Aged↗