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PubMed2005

[Dementia and driving: present status of drivers with dementia and response of their family's care in Japan].

As a result of the growing proportion of drivers aged 65 years and older, it is estimated that the number of elderly drivers with dementia is increasing in Japan. Since June 2002, if a driver is found to be "demented", his/her driving license shall be revoked in Japan. However, there are no consensus guidelines for demented drivers. Between September 1995 and September 2001, we evaluated 30 drivers with dementia (19 males and 11 females, mean age of 69.4 years) in out patients clinic of the Kochi Medical School Hospital and related hospitals. Clinical Diagnosis was Alzheimer's disease in 20, vascular dementia in 3, mixed type dementia in 2, frontotemporal lobar degeneration in 4, other type dementia in 1. We analyzed their driving behavior and family's attitude. Seventy-three point three percent of 30 drivers with dementia continued to drive after diagnosis. In follow-up periods, number of drivers continuing driving was decreased to 13 (43.3%), while six drivers (27.3%) had a traffic accident or violation. Our study suggests that several important medical and social factors should be considered for the management of drivers with dementia. A consensus medical guideline for demented drivers has to be established.

Accidents, Traffic↗
PubMed1981

[Multidisciplinary diagnosis of dementia and non-dementia behavior disorders in the aged. Preliminary study for research on its course and prognosis].

The need to differentiate between dementia and the so-called functional psychiatric diseases of old age is of therapeutic as well as social importance. The main symptoms of dementia--lack of memory, disorientation and cognitive disturbances--are much less clearly defined than would be desirable, despite the neuropathological changes regarded as underlying senile dementia. The disease does not always have a progressive course. Confusion is also possible with other forms of dementia, while the symptoms of dementia can also be found in so-called functional psychiatric diseases. On the basis of the literature and/of our own research, it appears that a sharper definition of senile dementia is possible. Besides clinical criteria one can make use of--partly recently introduced--diagnostic techniques, specifically a structured psychiatric interview for old people, a neuropsychological testbattery, EEG, visual evoked response techniques and CT-brain scanning. The value of these diagnostic techniques for the diagnosis and the assessment of the prognosis of senile dementia can only be determined in a follow-up study. The set-up of such a follow-up study is described.

Aged↗
PubMedDate not supplied

Amino acid concentration in dementia of the Alzheimer type and multi-infarct dementia.

Amino acids were measured in nine cases of dementia of the Alzheimer type, 10 cases of multi-infarct dementia, and 10 healthy controls. The severity of dementia was examined using mini-mental state test (MMST). Amino acid analysis (41 kinds) in the cerebrospinal fluid (CSF) and serum was performed in the Special Reference Laboratories. In the dementia of the Alzheimer type group, methionine and alanine concentrations in the CSF were significantly increased, and the CSF/serum ratios for both the alanine and glycine concentrations were significantly increased, in comparison with the healthy control group. In the multi-infarct dementia group, glycine, methionine, threonine, phenylalanine, and citrulline concentrations in the CSF were all higher than in the healthy control group. Significant negative correlations were found between the MMST score and the alanine, urea, arginine, and alpha-aminobutyric acid concentrations in the CSF. The number of amino acids which exhibited abnormality in dementia of the Alzheimer type and multi-infarct dementia was greater in the present study than in previous reports.

Aged↗
PubMed1996

[Role of Alzheimer's type dementia among dementias of the elderly].

In the authors experience of a memory clinic, about 2/3 of the patients fulfilled the criteria for dementia and among the demented patients 2/3 had probable Alzheimer's disease. Vascular dementia is the second cause of dementia in elderly people, but two other degenerative disorders fulfilling the NINCDS-ADRDA criteria for Alzheimer disease (Mc Khann et al., 1984) account for degenerative dementia. There is now a consensus for the clinical diagnosis and the neuropathological aspects of these two diseases: Dementia with Lewy Bodies (Mc Keith et al., 1996) and fronto-temporal dementia (the Lund and Manchester groups, 1994). The authors emphasize the clinical aspects of those two diseases at an early stage in comparison with dementia of Alzheimer type.

Aged↗
PubMedDate not supplied

[The prevalence of Alzheimer's type dementia and vascular dementia in the district of Swiebodzin].

In the study the prevalence of Alzheimer's type dementia and vascular dementia in the town of Swiebodzin and its surroundings was assessed. Also, the frequency of risk factors of vascular diseases for both types of dementia was evaluated. The study group comprised 7417 persons (45 years old and above). This population was divided into two groups. The younger subgroup (45-64 y) and the older one (65 y and above). The results obtained for indices of prevalence of both main types of dementia are comparable with the results that can be found in literature. The prevalence of Alzheimer's type dementia, in this study, is greater in women, while in men higher indices are referred to vascular dementia. The risk factors of cerebrovascular diseases are more frequent in the group of men. It could explain higher risk of vascular dementia in this group.

Aged↗
PubMed1998

Propentofylline in the treatment of vascular dementia and Alzheimer-type dementia: overview of phase I and phase II clinical trials.

Pathophysiologic processes common to both vascular (multi-infarct) dementia and dementia of the Alzheimer type may include microglial activation with resultant generation of inflammatory cytokines and neurotoxic free radicals, decreased secretion of nerve growth factor by astrocytes, excess release of glutamate with associated neurotoxicity, and loss of cholinergic neurons. The functional benefits and neuroprotective effects of propentofylline (PPF) stem from its interference with these overlapping pathways of neurodegeneration. The clinical pharmacology and safety of PPF were studied in a number of phase I studies in healthy young and elderly adults and in patients with renal or hepatic impairment. These studies have shown that PPF 300 mg t.i.d. is safe and well tolerated when taken on an empty stomach 1 h before meals. In a randomized, double-blind phase II study involving 190 elderly subjects with clinically and psychometrically documented mild to moderate dementia, 12 weeks of PPF therapy produced significantly greater improvements than placebo in Gottfries-Bråne-Steen (GBS) scores, Mini-Mental State Examination (MMSE) scores, and Clinical Global Impression (CGI) ratings. A subsequent phase II study using positron emission tomography (PET) revealed that cortical glucose metabolism improved significantly in patients with vascular dementia after 12 weeks of PPF treatment but deteriorated significantly with placebo. A third phase II study, which enrolled patients with Alzheimer-type dementia, demonstrated that PPF significantly enhanced functional reserve, as reflected by increases in regional cerebral glucose metabolism after stimulation with a verbal memory task. In contrast, patients randomized to placebo exhibited a significant decline in functional activation and significant worsening in their MMSE scores over the course of this 12-week study. Propentofylline proved to be safe, well tolerated, and free of severe side effects in all three of these phase II trials. Phase I trial results suggest that significant food interactions occur with PPF, indicating that the drug should be taken on an empty stomach 1 h before meals. Phase II trial results indicate that PPF yields clinically measurable improvements in the symptoms of dementia and prevents loss of stimulation-related increases in glucose metabolism over a treatment period of 3 months. Whether these results indicate that PPF can slow the progression of dementia can be determined only by long-term trials specifically designed to determine the drug's effect on disease progression.

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PubMed2002

[Managing patients with dementia--current status and formulating dementia policy desiderata and options ].

The demographic and epidemiological scenarios, concerning persons with dementia, are in tension between the legal general conditions of care, on the one hand, and the conceptual alignment, on the other hand; this tension is hardly resolved by the momentary activities in health and care policy. Even on the level of assessment, there are scarcely any instruments to picture the specific needs of patients with dementia. Concepts of supply for persons with dementia are widely still divided by the differentiation between stationary and outpatient. Intelligent mixtures and paradigmatic reorientation towards normalization or split responsibility have not yet enfolded their embossing effects in practice. The care of persons with dementia is in many respects still bound in pre-technical constellations: this applies to the conceptual bias inside an institution or service of old people's care, to legal and economical general conditions and instruments of control and in many ways also to the technical discourse. The relevancy of attendance of people with dementia today and in the future justifies talking about "dementia policy". Options for dementia policy lay in a consequent adaptation of the theory of the New Welfare Mix, which was developed by the political sciences, including discussion about normalization in the area of help for disabled people and in the reformulation of competence between the means of fringe benefits and employees' benefits in joint responsibility.

Aged↗
PubMed2004

Survival following dementia onset: Alzheimer's disease and vascular dementia.

Survival following the onset of dementia has been reported to vary from 3 to over 9 years. We examined mortality in 3602 participants of the Cardiovascular Health (CHS) Cognition Study in four US communities evaluated for dementia incidence between 1992 and 1999 and followed for 6.5 years. By June 2000, 33 of 62 (53.2%) participants who developed vascular dementia (VaD) had died compared to 79 of 245 (32.2%) with Alzheimer's disease (AD), 66 of 151 (43.7%) with both AD and VaD, and 429 of 2318 (18.5%) with normal cognition. Using Cox proportional hazards regression with a time-dependent covariate for dementia status adjusted for age, gender and race, individuals with VaD were more than four times as likely to die during follow-up than those with normal cognition (HR: 4.4, 95% CI: 3.1-6.3). The hazard ratios were 2.1 (95% CI: 1.6-2.7) for AD and 2.5 (95% CI: 1.9-3.3) for both types. Adjusted accelerated life models estimated median survival from dementia onset to death as 3.9 years for those with VaD, 7.1 years for AD, 5.4 years for mixed dementia, and 11.0 years for matched controls with normal cognition. While persons with VaD died primarily from cerebrovascular disease, those with AD/mixed dementia died more frequently from dementia/failure to thrive.

Aged↗
PubMed2000

Spectrum of Parkinson's disease, Parkinson's dementia, and Lewy body dementia.

Dementia occurs more commonly in individuals with Parkinson's disease (PD) than in the age-matched general population. Dementia in PD may result from a mixture of cortical and subcortical dementia syndromes caused by a variety of underlying pathologic processes and neurochemical deficits. A primary dementia syndrome has been described that shares several pathologic and clinical characteristics with PD. Dementia with Lewy bodies (DLB) accounts for 15% to 20% of all dementia syndromes in old age, which makes it second only to Alzheimer's disease in prevalence. The relationship between dementia in PD and DLB has not been fully resolved but may be considered useful in terms of neuropathologic substrate, clinical features, and response to treatment.

Aged↗
PubMed2001

Measuring the well-being of people with dementia living in formal care settings: the use of Dementia Care Mapping.

Over the years there have been advances in the quality of care provision for people with dementia. How to measure the impact of care on the person with dementia has challenged researchers as, until recently, no evaluation tool offered a comprehensive overview of the behaviour patterns and well-being of persons with dementia. Dementia Care Mapping (DCM) is a tool used by care practitioners and researchers to capture both the process (behaviours) and outcome (well-being) of care and is therefore of use as a tool to evaluate quality of care. This study aims to assess, through DCM, the experience of dementia care provision in residential and nursing homes in two voluntary organizations in England. The data illustrates similarities in the well-being and behaviour patterns of 76 persons with dementia living in six care settings throughout England. Examples of instances when people with dementia were "put down" and when well-being was enhanced, are outlined. The homes in the study were meeting the physical care but not the broader psychosocial care needs of the observed residents. The action taken by the organizations as a result of the DCM evaluations is summarized.

Aged↗
PubMed2001

Alcohol dementia: "cortical" or "subcortical" dementia?

Most dementias are considered to exhibit either a predominantly "cortical" (e.g. Alzheimer's disease, AD) or "subcortical" (e.g. Parkinson's disease) pattern. A double dissociation has been reported, such that cortical and subcortical dementias can be differentiated based on performance on tests of declarative and procedural learning. The goal of this study was to determine if subjects with alcohol dementia exhibit a predominantly cortical or subcortical dementia profile. The performance of 10 elderly subjects diagnosed with alcohol dementia, 29 elderly subjects with histories of alcohol dependence but who were not demented, and 11 subjects with AD was compared to 20 elderly control subjects. The results indicated that the procedural learning task did not differentiate among the groups, whereas the discriminability index from the California Learning Test (the declarative learning task) did. Thus, alcohol dementia cannot clearly be ascribed to either dementia classification.

Journal Article↗
PubMed2005

"Forme fruste" of amyotrophic lateral sclerosis with dementia: a report of five autopsy cases without dementia and with ubiquitinated intraneuronal inclusions.

We clinicopathologically investigated five autopsy cases of ALS without dementia and with ubiquitinated intraneuronal inclusions. The age at onset of symptoms ranged from 52 to 81 years and the duration of the disease was from 10 months to 3 years, 3 months. All five patients initially developed lower motor neuron signs, including bulbar signs, and upper motor neuron signs were found in the middle to late clinical stages, but dementia was not observed in all five cases. Thus, the clinical diagnoses of all five patients were ALS without dementia. Neuropathological examination of all five cases revealed not only obvious degeneration of upper motor neurons with neuronal loss of Betz cells, but also lower motor neuron involvement associated with Bunina bodies. In addition, ubiquitin-immunoreactive intraneuronal inclusions in the hippocampal dentate granular cells and degeneration of the substantia nigra were observed in all five cases. Furthermore, neuronal loss with astrocytosis in the dorsomedial portion of the anterior first temporal gyrus was observed in all three cases in which this structure was examined. Neuronal loss with astrocytosis in the subiculum was found in four cases. Neuronal loss of the parahippocampal gyrus was observed in three of the five autopsy cases, and amygdala involvement was encountered in three of four cases in which this structure was investigated. Based on these clinicopathological findings and a review of the published literature, we concluded that our five cases were ALS without dementia, but with pathological hallmarks compatible with ALS with dementia. We also concluded that there is a "forme fruste" of ALS with dementia showing no overt dementia clinically.

Age of Onset↗
PubMed2006

MRI and SPECT studies of dural arteriovenous fistulas presenting as pure progressive dementia with leukoencephalopathy: a cause of treatable dementia.

We report two patients with dural arteriovenous fistulas (DAVFs) who presented with pure progressive dementia. Both patients showed only slowly progressive dementia, without headache, papilledema and other neurologic signs associated with diffuse white matter changes in MRI. MR cerebral angiography showed sigmoid sinus DAVFs that were mainly supplied by the occipital artery, together with retrograde filling of the superior sagittal and straight sinus and dilated cortical veins. SPECT studies showed extensive blood flow reduction in the occipital and parieto-occipital areas and right temporal lobe in one patient. Selective embolization for treatment of the DAVF improved cognitive function associated with the abnormal white matter MRI signal. MRI and SPECT showed that severity of dementia correlated with diffuse white matter changes and regional cerebral blood flow. Our cases suggest that gradually impaired cerebral circulation due to venous hypertensive encephalopathy could be involved in slowly progressive dementia with leukoencephalopathy resulting from a DAVF. DAVFs may be particularly important for differential diagnosis in elderly patients with pure progressive dementia. Thus, early diagnosis of DAVFs and treatment by endovascular surgery is important as treatable or reversible dementia.

Central Nervous System Vascular Malformations↗
PubMedDate not supplied

Response to activated protein C in subjects with and without dementia. The Dutch Vascular Factors in Dementia Study.

We performed a cross-sectional case-control study among 295 subjects with dementia and 406 control subjects drawn from participants of the Rotterdam Study, a population-based cohort study among subjects aged 55 years or over, and from participants of the Rotterdam Stroke Databank, a hospital-based stroke registry, to evaluate the association of the factor V Leiden mutation and activated protein C (APC) response with dementia and its subtypes. The risk of dementia was 2.11-fold increased among carriers of factor V Leiden mutation relative to subjects lacking factor V Leiden mutation (95% confidence interval, CI, 0.93-4.77). The increased risks of vascular dementia and of Alzheimer's disease were 4.28 (95% CI 1.26-14.5) and 2.15 (95% CI 0.82-5.63), respectively. No association was found for APC response. We showed a nonsignificant twofold increased risk of dementia among subjects with factor V Leiden. The association appeared to be stronger for vascular dementia.

Activated Protein C Resistance↗
PubMed2002

[Binswanger's disease or multi-infarct dementia? Diagnostic keys in vascular dementia].

OBJECTIVE: To develop a model that assists in the classification of patients with vascular dementia in two of its most relevant subtypes: multi-infarct dementia (cortical involvement) and Binswanger's disease (subcortical involvement). PATIENTS AND METHODS: Retrospective analysis of 50 consecutive patients with Binswanger's disease and 50 patients with multi-infarct dementia studied throughout a 12-year period (1986-1998) in a tertiary university hospital. The statistical model was obtained by multivariant analysis (logit model) and its accuracy was estimated by means of ROC curve analysis. RESULTS: The variables included in the regression model were: arterial hypertension (p < 0.03), cardioembolic disease (p < 0.05), and presence of cortical (p < 0.01) and lacunar (p < 0.01) infarctions in CAT. The specificity of the model was 90%, the sensitivity near 60%, and the positive likelihood ratio 5.8. The area under the ROC curve was 0.80 (0.73-0.87). CONCLUSIONS: Despite the availability of consensus diagnostic criteria for vascular dementia, their use is very commonly restricted to the research field. We have developed a classification model for patients with vascular dementia in two relevant subgroups: multi-infarct dementia and Binswanger's disease. This model can contribute to make identification of these patients in the daily clinical practice easier.

Dementia, Multi-Infarct↗
PubMed1987

Senile dementia of the Binswanger type. A vascular form of dementia in the elderly.

Computed tomography and magnetic resonance imaging in the elderly have demonstrated the common occurrence of deep white-matter lesions in the aging brain. These radiologic lesions (leukoaraiosis) may represent an early marker of dementia. At autopsy, an ischemic periventricular leukoencephalopathy (Binswanger's disease) has been found in most cases. The clinical spectrum of Binswanger's disease appears to range from asymptomatic radiologic lesions to dementia with focal deficits, frontal signs, pseudobulbar palsy, gait difficulties, and urinary incontinence. The name senile dementia of the Binswanger type (SDBT) is proposed for this poorly recognized, vascular form of subcortical dementia. The SDBT probably results from cortical disconnection most likely caused by hypoperfusion. In contrast, multi-infarct dementia is correlated with multiple large and small strokes that cause a loss of over 50 to 100 mL of brain volume. The periventricular white matter is a watershed area irrigated by long, penetrating medullary arteries. Risk factors for SDBT are small-artery diseases, such as hypertension and amyloid angiopathy, impaired autoregulation of cerebral blood flow in the elderly, and periventricular hypoperfusion due to cardiac failure, arrhythmias, and hypotension. The SDBT may be a potentially preventable and treatable form of dementia.

Aged↗
PubMed2000

Methodological issues for population-based research into dementia in developing countries. A position paper from the 10/66 Dementia Research Group.

The 10/66 Dementia Research Group has been formed to promote good-quality, internationally comparable research into dementia in developing countries through active research collaboration. In this position paper, we review existing research into dementia prevalence in developing regions of the world. Seven methodologically robust studies were identified. The prevalence of dementia, age-adjusted to the age structure of the Kerala population, ranged from 1.3% to 5.3% for all those aged 60 or over and from 1.7% to 5.2% for all those aged 65 and over. Two studies, from Ibadan, Nigeria and Ballabgarh, India, reported strikingly low prevalence figures. The reported prevalence for most studies was somewhat lower than the consistent figures for Europe reported by the EURODEM concerted action. Based on critical review of the literature, and on the practical research experience of members of the 10/66 group, recommendations have been made for procedure in the following areas: age limits for inclusion in dementia surveys, age ascertainment, sampling, scope for incidence studies, functional assessment and culture- and education-fair dementia diagnosis.

Age Distribution↗
PubMed1998

Age and dementia effect on neuropsychological test performance in very old age--influence of risk factors for dementia.

In old age a large part of the variance in cognitive performance in population samples is explained by normal aging; in addition many subjects over 80 years are demented and therefore dementia also explains a part of cognitive variability. The question is whether the different factors for dementia (such as ApoE4, external atrophy parameter of the cranial computer tomography [cCT], education, sex or serum zinc level) influence the relation between age or dementia and Mini Mental State (MMSE) performance. In an epidemiological study data were analyzed of N = 239 subjects for the above factors. Most statistically significant variables of the MMSE do not change the amount of the partial correlation coefficient between the parameters age or dementia and MMSE. The external atrophy, however, diminishes the magnitude of the partial correlation between age and MMSE. In contrast the dementia-MMSE relation is unchanged. This points to a generally similar factor structure of cognitive aging and dementia in old age, but differences exist with respect to the importance of the external atrophy parameter of the brain. Most factors investigated explain separate parts of variance of cognitive performance in old age.

Adult↗