{"title":"Deterioration of spontaneous speech in AD patients during a 1-year follow-up: homogeneity of profiles and factors associated with progression.","authors":"B Romero, A Kurz","doi":"10.1159/000106850","DOIUrl":"https://doi.org/10.1159/000106850","url":null,"abstract":"<p><p>This longitudinal study measured the rate of spontaneous speech decline in patients with Alzheimer's disease (AD) at a 1-year follow-up and determined the effect of clinical and demographic factors on that rate. In addition the pattern of spontaneous speech impairment was examined. The expected pattern of spontaneous speech impairment with prominent disturbances of communication and semantics, moderate disturbances of automatic speech, but with retained phonematic structures, was found at baseline and at follow-up in the majority of our rather large sample (n = 63). This result is discussed in terms of intrafunctional homogeneity and of selective involvement of neuronal systems in AD. There was a trend for a more rapid language decline in patients with a family history of dementia. No relationship was detected between the rate of spontaneous speech decline and other clinical and demographic factors, with the exception of initial spontaneous speech impairment.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"7 1","pages":"35-40"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106850","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19759411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Senile dementia of Alzheimer type and multi-infarct dementia investigated by transcranial Doppler sonography.","authors":"H Sattel, H Förstl, S Biedert","doi":"10.1159/000106851","DOIUrl":"https://doi.org/10.1159/000106851","url":null,"abstract":"<p><p>Dementia of the Alzheimer type, senile onset (SDAT), and multi-infarct dementia (MID) exhibit differences in cerebrovascular blood flow velocity profiles, which were investigated by means of transcranial Doppler sonography. The pulsatility indices (PI), as angle-independent parameters of peripheral vascular resistance measured in the basal cerebral arteries, were significantly increased in MID patients with respect to SDAT cases. In an analysis of the correlations between several variables and the magnitude of PI, we found strong inverse correlations of the CAMCOG score, and strong direct correlations of the blood pressure and the duration of illness, with the PI of all basal cerebral arteries only in MID patients. In SDAT patients, we found a direct correlation between the Hachinski ischemia score and the PI of all basal cerebral arteries. All 3 ischemia scores (Hachinski, Rosen, Loeb and Gandolfo) were significantly correlated with the PI of the middle cerebral and basilar arteries. By analyzing the correlations of the single items of the 3 different ischemia scores with the PI values obtained, we only found a clearcut correlation with the item focal neurological signs. Thus, our findings stress the relative importance of a concomitant cerebrovascular factor in the development of dementia in old age, even in patients with probable SDAT. A raise of the PI in the basal cerebral arteries allows early suspicion of a cerebrovascular factor even in only slight dementia so that possible risk factors for further aggravation of this type of vascular dementia might be detected and treated early in the course of disease.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"7 1","pages":"41-6"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106851","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19759413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
H Förstl, C Besthorn, F Hentschel, C Geiger-Kabisch, H Sattel, U Schreiter-Gasser
{"title":"Frontal lobe degeneration and Alzheimer's disease: a controlled study on clinical findings, volumetric brain changes and quantitative electroencephalography data.","authors":"H Förstl, C Besthorn, F Hentschel, C Geiger-Kabisch, H Sattel, U Schreiter-Gasser","doi":"10.1159/000106849","DOIUrl":"https://doi.org/10.1159/000106849","url":null,"abstract":"<p><p>Ten patients with a clinical diagnosis of frontal lobe degeneration (FLD) were compared with a group of patients with probable Alzheimer's disease (AD) and with nondemented controls matched for gender and age. In comparison with AD, the duration of illness was slightly shorter and cognitive performance was better in patients with FLD. The greatest enlargement of cerebrospinal fluid volumes was found in FLD and this effect was most pronounced in the anterior fissure and lateral ventricles. Estimates of EEG band-power and EEG coherence in FLD were not remarkably different from nondemented controls, whereas delta- and theta-power were significantly increased in AD. These observations may indicate different disease processes with a dissociation of volumetric computed tomography and quantitative EEG changes, which may be of differential diagnostic value.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"7 1","pages":"27-34"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106849","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19758889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J Snaedal, T Johannesson, J E Jonsson, G Gylfadottir
{"title":"The effects of nicotine in dermal plaster on cognitive functions in patients with Alzheimer's disease.","authors":"J Snaedal, T Johannesson, J E Jonsson, G Gylfadottir","doi":"10.1159/000106852","DOIUrl":"https://doi.org/10.1159/000106852","url":null,"abstract":"<p><p>Eighteen patients with probable Alzheimer's disease (NINCDS/ADRDA criteria) participated in a placebo-controlled, double-blind study, with a crossover design. The patients had mild or moderate dementia (MMSE = 20.3 +/- 4.6, range 12-28). The trial consisted of two 4-week periods with a 2-week washout period in between. Nicotine was given in the form of dermal plasters. Most of the patients tolerated the highest doses of 21 mg nicotine/24 h, but some received 14 mg/24 h. The effect was monitored with tests of short-term memory, verbal fluency, attention and psychomotor speed. Nicotine was also determined in the blood. Short-term memory improved significantly after 4 weeks of treatment, both on nicotine and placebo (p < 0.05/p < 0.01). The results of our study thus do not indicate that nicotine applied in the form of dermal plasters is of any significance in the treatment of memory deficits in patient with Alzheimer's disease.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"7 1","pages":"47-52"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106852","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19759416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
G B Frisoni, A Beltramello, C Weiss, C Geroldi, A Bianchetti, M Trabucchi
{"title":"Usefulness of simple measures of temporal lobe atrophy in probable Alzheimer's disease.","authors":"G B Frisoni, A Beltramello, C Weiss, C Geroldi, A Bianchetti, M Trabucchi","doi":"10.1159/000106847","DOIUrl":"https://doi.org/10.1159/000106847","url":null,"abstract":"<p><p>Diagnosis of Alzheimer's disease is made on clinical grounds, and the availability of a simple and sensitive quantitative index of the disease might aid in the routine diagnosis. The aim of this study was to assess whether linear measures of brain atrophy as detected by magnetic resonance imaging can be helpful in the differentiation of mild to moderate Alzheimer's disease from nondemented elderly. Measures of global (bifrontal index and interuncal distance) and hippocampal (minimum thickness of the medial temporal lobe, hippocampal height, width of the choroid fissure, and width of the temporal horn) atrophy were taken from 26 cases and 21 controls. Measures of hippocampal atrophy were the most sensitive in the differentiation of cases from controls, and among them width of the temporal horn yielded the highest sensitivity, predicting the disease in 73% of cases with 95% specificity. A compound measure comprising width of the temporal horn, width of the choroid fissure, and hippocampal height increased sensitivity to 85%. These results suggest that selected simple indices of hippocampal atrophy might be useful in the diagnosis of Alzheimer's disease.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"7 1","pages":"15-22"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106847","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19758887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Aphasia, apraxia, and agnosia in the diagnosis of dementia.","authors":"J H Kramer, J M Duffy","doi":"10.1159/000106848","DOIUrl":"https://doi.org/10.1159/000106848","url":null,"abstract":"<p><p>The association of aphasia, apraxia and agnosia with cortical but not subcortical dementias, is a widely held belief. The purpose of the present study was to determine the frequency of aphasia, apraxia, and agnosia in groups of cortical and subcortical dementia patients, and to assess the diagnostic utility of these symptoms. Subjects were 64 patients with subcortical dementias (Parkinson's disease and normal pressure hydrocephalus) and 192 patients with cortical dementia (probable Alzheimer's disease) matched for sex, age, and Mini-Mental State Examination score. Each patient was evaluated for the presence of aphasia, apraxia, and agnosia. Results indicated that only aphasia was reported significantly more often in cortical dementia patients than in subcortical dementia patients. The presence of either of these three symptoms has very low diagnostic sensitivity, specificity, and total predictive value. The severity of the patient's dementia was predicted whether the patient had aphasia or apraxia; type of dementia had no predictive value. These data led to the conclusion that cortical and subcortical dementias cannot be reliably dissociated on the basis of aphasia, apraxia, or agnosia.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"7 1","pages":"23-6"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106848","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19758888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Aluminium and Alzheimer's disease: review of possible pathogenic mechanisms.","authors":"R A Armstrong, S J Winsper, J A Blair","doi":"10.1159/000106845","DOIUrl":"https://doi.org/10.1159/000106845","url":null,"abstract":"<p><p>Chronic exposure to aluminium (Al) remains a controversial possible cause of sporadic forms of Alzheimer's disease (AD). This article reviews the evidence that once Al enters the brain and individual brain cells, it may be involved in three pathological processes: (1) the production of abnormal forms of tau leading to the formation of cellular neurofibrillary tangles and neuropil threads; (2) the processing of the amyloid precursor protein, resulting in the formation of beta-amyloid deposits and senile plaques, and (3) that via the mutual histocompatibility system, Al could be involved in the initiation of the immune response observed in AD patients. Despite recent evidence that Al could be involved in these processes, a conclusive case that exposure to Al initiates the primary pathological process in sporadic AD remains to be established.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"7 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106845","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19758885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Chromogranin A in cerebrospinal fluid: a biochemical marker for synaptic degeneration in Alzheimer's disease?","authors":"K Blennow, P Davidsson, A Wallin, R Ekman","doi":"10.1159/000106963","DOIUrl":"https://doi.org/10.1159/000106963","url":null,"abstract":"<p><p>Biochemical markers for AD would be of great value both to improve the clinical diagnostic accuracy in scientific studies and to increase the knowledge of the pathogenesis of the disorder. One of the main features of AD is a degeneration of synapses. Therefore, we examined if chromogranin A (CrA), the major protein of large dense-core synaptic vesicles, in cerebrospinal fluid (CSF) may be of value as a biochemical marker for the synaptic function in AD. The mean concentration of CrA in CSF was about 7.5 times higher than its concentration in serum, and there was no significant correlation between CSF-CrA and the blood-brain barrier function (measured as the CSF/serum albumin ratio), nor between CSF-CrA and serum-CrA. These findings suggest that the major portion of CSF-CrA is locally produced within the CNS. There were no significant differences in CSF-CrA between the AD (n = 29), vascular dementia (n = 13), and age-matched control (n = 9) groups (99.9 +/- 58.9 ng/ml, 108.0 +/- 69.4 ng/ml, and 115.1 +/- 44.4 ng/ml, respectively). However, when the AD group was subdivided into AD type I (n = 12) and AD type II (n = 17), a lower concentration of CSF-CrA was found in AD type I (72.8 +/- 28.9 ng/ml) compared with controls (115.1 +/- 44.4 ng/ml), p < 0.02, and compared with AD type II (119.1 +/- 67.5 ng/ml), p < 0.05, while CSF-CrA did not significantly differ between AD type II and controls. These findings suggest that CSF-CrA has a potential as a biochemical marker for the synaptic degeneration in AD type I, and gives further support for the relevance of identifying the AD type I (pure AD) subgroup in scientific studies.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"6 6","pages":"306-11"},"PeriodicalIF":0.0,"publicationDate":"1995-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106963","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19544464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"EEG findings in dementia are related to the parietal lobe syndrome.","authors":"A Edman, M Matousek, A Wallin","doi":"10.1159/000106965","DOIUrl":"https://doi.org/10.1159/000106965","url":null,"abstract":"<p><p>EEG indicators were correlated with clinical items in 174 patients with dementia diagnoses based on the DSM-III-R criteria. The patients' clinical symptomatologies were presented as regional brain syndromes, i.e. parietal lobe, frontal lobe, subcortical and global (nonregional) syndromes. The EEGs were abnormal in 87% of the cases. The typical abnormalities consisted of diffusely distributed slow wave activity. A significant correlation was found between the degree of slow wave abnormality and the degree of dementia. The results of the statistical analysis also suggest that EEG slow wave activity in dementia primarily reflects parietal lobe dysfunction. No association seems to exist between EEG slow wave activity and frontal lobe dysfunction.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"6 6","pages":"323-9"},"PeriodicalIF":0.0,"publicationDate":"1995-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106965","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19544466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Number of platelet dense granules varies with age, schizophrenia and dementia.","authors":"A Kessler, M Shinitzky, B Kessler","doi":"10.1159/000106966","DOIUrl":"https://doi.org/10.1159/000106966","url":null,"abstract":"<p><p>In the present study we observed that the number of dense granules per platelet increases with age, attaining a maximum level above the age of about 40 years. Platelets of newborns apparently contain only a small number of dense granules per platelet. The numbers of platelet dense granules and platelet cell size in schizophrenic patients increase compared to age-matched healthy controls. In contrast, in Alzheimer-type dementia the number of platelet dense granules tends to decrease compared to healthy persons.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"6 6","pages":"330-3"},"PeriodicalIF":0.0,"publicationDate":"1995-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106966","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19544359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}