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K Marder

Publications and source records attributed to K Marder.

139 records · Page 8Linked to original sources
PubMed1992

Event-related potentials (ERPs) during repetition priming in Alzheimer's patients and young and older controls.

Although memory tested explicitly (e.g., recognition) is clearly deficient in the early stages of Alzheimer's disease, it is less clear if memory tested implicitly is similarly affected. To assess this, event-related potentials (ERPs) were recorded during a word-repetition priming paradigm, with semantic and orthographic orienting tasks, from 10 patients with mild probable Alzheimer's disease (PAD; mean age of 70.6), 10 young (24.1) and 10 older (69.8) controls. The extent of priming by word repetition was assessed using the new minus old ERP repetition effect. The young and older control groups showed clear ERP repetition effects that were larger during semantic than orthographic blocks. Although the PAD patients displayed the same general trends, their ERP repetition effects were not nearly as marked when compared to controls. To the extent that the ERP repetition effect recorded during this repetition priming paradigm is a measure of implicit performance, the data suggest that memory assessed in this fashion is spared in at least some Alzheimer's patients in the early stages of the disease.

Adult↗
PubMed1991

Tritiated imipramine binding. A peripheral marker for serotonin in Parkinson's disease.

Tritiated imipramine binding in platelets has been used to evaluate serotonin activity in depression in previous studies. This article examined this marker as a possible measure of central nervous system serotonergic activity for depression in patients with Parkinson's disease (PD). The number of binding sites was significantly lower in depressed patients with PD than in a healthy control group. Patients with PD who were not depressed had lower values than the comparison group, but this difference was not significant. We also found a significant correlation between the receptor site values in platelets and cerebrospinal fluid levels of the serotonin metabolite, 5-hydroxyindoleacetic acid (r = .59), but this was independent of a diagnosis of depression. Receptor site values were examined to identify appropriate cutoff scores to predict depression in the group of patients with PD. A maximum sensitivity of 50% was achieved with a specificity of 64%. Our results strongly support a generalized alteration in serotonin metabolism in depressed patients with PD, but tritiated imipramine binding in platelets is not a useful diagnostic tool for depression.

Aged↗
PubMed1991

Interrater reliability of extrapyramidal signs in a group assessed for dementia.

Extrapyramidal signs were rated by three neurologists in 20 patients who had either been diagnosed as having probable Alzheimer's disease or who were being evaluated for dementia. In general, good interrater reliability was found for the presence or absence of extrapyramidal signs, although agreement over the presence of some signs was reduced when distinctions between normality and slight departures from normality were required.

Aged↗
PubMed1991

Multidisciplinary baseline assessment of homosexual men with and without human immunodeficiency virus infection. III. Neurologic and neuropsychological findings.

We explored the possibility that neurologic and neuropsychological changes constitute the earliest detectable manifestations of human immunodeficiency virus (HIV) infection. Without knowledge of HIV status, we assessed neurologic signs and symptoms and administered a battery of neuropsychological tests to 208 homosexual men, of whom 84 were HIV negative, 49 were HIV positive and asymptomatic, 29 were mildly symptomatic, and 46 had significant medical symptoms but not the acquired immunodeficiency syndrome. There was no difference between the HIV-negative and HIV-positive men in the frequency of neurologic signs or of defective or borderline performance on any neuropsychological test. However, HIV-positive men performed slightly but significantly worse than HIV-negative men on tests of verbal memory, executive function, and language. Similar results were obtained when comparisons were limited to HIV-positive medically asymptomatic and HIV-negative men. There was no degradation of neurologic status or neuropsychological performance across stages of HIV severity, but neurologic and neuropsychological summary scores correlated with CD4/CD8 ratios in the HIV-positive group. Ratings of neurologic signs and symptoms correlated with neuropsychological summary scores in the HIV-positive group only. Cognitive complaints were more frequent in the HIV-positive men; they correlated with actual test performance in the HIV-positive but not HIV-negative men. The constellation of subjective and objective neuropsychological and neurologic findings suggests the possibility of a definable syndrome associated with HIV infection in asymptomatic individuals.

Adolescent↗
PubMed1991

Codon 618 variant of Alzheimer amyloid gene associated with inherited cerebral hemorrhage.

Hereditary cerebral hemorrhage with amyloidosis, Dutch type (HCHWA-D) is an autosomal dominant form of severe cerebrovascular amyloid angiopathy causing recurrent strokes during the fifth and sixth decades of life. The major constituent of the amyloid deposits in HCHWA-D is the amyloid beta-protein (A beta), also found in Alzheimer's disease. A point mutation in the DNA sequence encoding A beta has been found in 2 unrelated patients with HCHWA-D, and an assay detecting the single base change was developed for diagnostic purposes. We describe the detection of the point mutation in a patient living in the United States, suffering from recurring cerebral hemorrhages, who only recently was diagnosed with HCHWA-D. In addition, we tested a number of family members, and found the mutation in 2 additional individuals, one of them too young to exhibit clinical manifestations. This study combined with the study of two other families in Holland indicates that the codon 618 variant in the amyloid precursor protein gene segregates with HCHWA-D.

Aged↗
PubMed1991

Are demented patients with Parkinson's disease accurately reflected in prevalence surveys? A survival analysis.

We re-reviewed 257 patient records previously reviewed for an incidence study of dementia in Parkinson's disease (PD) to determine the frequency, date of death, and cause of death. We posited that if disease duration is shortened when dementia occurs, then dementia may be far more common than reflected in prevalence studies. There were 17 deaths among 65 demented patients and 28 deaths among 168 nondemented patients. When we matched a subset of the nondemented patients to the demented patients by age and disease duration distributions, the demented subjects had significantly more deaths (p less than 0.02), and survival among demented subjects was decreased (p less than 0.05). Dementia was a significant predictor of death in this sample. We conclude that dementia reduces survival in patients with PD. Incidence is a much better measure of dementia in PD than prevalence because shortened duration makes it less likely to detect dementia in prevalence surveys.

Aged↗
PubMed1990

A pilot study of risk factors for dementia in Parkinson's disease.

To determine whether the risk factors for dementia in idiopathic Parkinson's disease (IPD) are similar to the risk factors for Alzheimer's disease, we conducted a case-control study of potential risk factors. A structured interview was administered to surrogates of 17 demented subjects with IPD and 54 nondemented subjects. Two factors emerged as possible risks for dementia. Demented patients were older than nondemented patients, although the duration of symptoms was similar. A family history of dementia was present in 30% of the demented group and 5.6% of the nondemented group. Dementia was most often reported among siblings. No difference was seen in toxic and occupational exposure, personal habits, or medical or surgical illnesses. We conclude that dementia in IPD shares some common risk factors with Alzheimer's disease. Efforts to assess the contribution of genetic susceptibility or shared environmental influences may clarify the relationship between these two diseases.

Aged↗
PubMed1990

A controlled trial of piracetam in intellectually impaired patients with Parkinson's disease.

Twenty patients with Parkinson's disease and marked intellectual impairment or dementia participated in a double-blind placebo controlled trial of the nootropic, piracetam. A standardized neurological examination, a neuropsychological test battery, and a functional scale, The Sickness Impact Profile, were completed for all patients. They were then assigned by blind randomization to drug or placebo conditions receiving 3.2 g of piracetam or an identical amount of placebo for 12 weeks. The dose was increased to 4.8 g for an additional 12 weeks. Neurological, psychological, and functional measures were rated as improved, unchanged, or worsened in comparison to baseline performance. Twenty-five percent of the patients did not complete the trial for reasons unrelated to the medication. Although there was a significant improvement on one subtest of the functional scale, no significant effects were demonstrated in cognitive or neurological measures.

Aged↗
PubMed1990

An estimate of the incidence of dementia in idiopathic Parkinson's disease.

The proportion of patients with idiopathic Parkinson's disease (PD) who are considered demented ranges from 10% to 15%. Because dementia may affect survival in PD, the incidence rate of dementia, rather than proportion, would be a more accurate measure of disease frequency. We previously estimated the proportion of patients with PD and dementia to be 10.9% from the records of a cohort with the idiopathic form of PD in a major medical center. We reviewed the clinical records of this cohort after 4 years and 9 months to estimate the incidence rate of dementia. We identified 65 new cases of dementia from the 249 patient-records available. Using the number of person-years of follow-up for each case as the denominator, we estimated the overall incidence rate to be 69 per 1,000 person-years of observation. The mean age of this cohort was 71.4 years. The cumulative incidence of dementia increased with age. By 85 years of age, over 65% of the surviving members of the cohort were demented. The age-specific incidence rates for dementia in this cohort of PD were significantly greater than for a similarly aged cohort of healthy elderly people. The age-specific standard morbidity ratios indicated that, compared with people of similar ages, patients with PD have the highest increase in risk for dementia between ages 65 and 75.

Age Factors↗
PubMed1988

An estimate of the prevalence of dementia in idiopathic Parkinson's disease.

A review of the records for evidence of dementia using criteria adapted from the third edition of the Diagnostic and Statistical Manual of Mental Disorders in every patient (hospitalized and outpatient) with parkinsonism at a major medical center during an 18-month period revealed an overall prevalence of 10.9% in 339 patients with idiopathic Parkinson's disease. Demented patients were older, had a later age at onset of motor manifestations, and a more rapid progression of physical disability than nondemented patients. Duration of illness and levodopa use and the presence of tremor or depression were similar in demented and nondemented patients. Demented patients more often responded poorly or developed adverse effects to levodopa than nondemented patients. When Parkinson's disease began after age 70 years, dementia was noted over three times more frequently than when the disease began at an earlier age. The age-specific prevalence rate of dementia for patients older than 70 years was more than twice that for younger patients. Moreover, the number of records with evidence for dementia with idiopathic Parkinson's disease was 3.75 times greater than expected in comparison with data from a study of the prevalence of dementia in the elderly.

Aged↗
PubMed1980

Acquisition of visuomotor behavior after neonatal tectal lesions in the hamster: the role of visual experience.

After neonatal damage to the midbrain tectum, hamsters exhibit as adults substantially reorganized retinal projections to the thalamus and midbrain. These experiments investigated the pattern of acquisition of a range of visuomotor capacities in hamsters with neonatal tectal damage, and the role of visual experience in this acquisition, by examining the time course of visuomotor development and the effects of dark-rearing on visuomotor behavior. These hamsters acquired visual orientation and pursuit at the same age as normal hamsters, but orientation and pursuit were impaired and exhibited no improvement over time. Photophobia and edge and depth sensitivity were relatively unaffected. Dark-rearing disrupted all visuomotor behavior in the midbrain-damage animals but had no effect on normal animals. These results are consistent with a dominant role of neocortex in the residual visuomotor capacities of animals with neonatal ablations of the midbrain tectum.

Animals↗