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Signal transduction mechanisms in memory disorders.
This chapter explores some of the molecular events contributing to memory formation and how, when these events malfunction, disturbances in memory occur. After a brief discussion of signaling in the hippocampus, we will explore the topics of human mental retardation syndromes that involve disruption of these processes, including Angelman syndrome (AS), Neurofibromatosis 1 (NF1)-associated learning disorders, Coffin-Lowry syndrome (CLS), Rubinstein-Taybi syndrome (RTS), and Rett syndrome (RTT).
Cued recall and the nature of the memory disorder in dementia.
The study investigated the retrieval deficit hypothesis of forgetting in senile dementia, using a cued recall technique. Memory for lists of words was tested with either no cues given at the time of recall, or alternatively by cueing the patient either with the word's first letter or its semantic category. Results do not support a retrieval deficit explanation of forgetting in dementia, but instead suggest the possibility of a processing deficit at the acquisition stage.
Cholinergic underactivity in human memory disorders.
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[Experimental memory disorders and their pharmacologic correction].
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A brief survey of the management of memory disorders in rehabilitation units in Britain.
A survey of rehabilitation units and other hospitals and departments involved in the management of memory dysfunction revealed considerable variation in approaches to treatment and in assessment techniques. A very few respondents with a special interest in memory dysfunction were used wide ranges of tests, training procedures and aids. Other respondents were concerned about the lack of training and in the management of memory problems and the lack of guidance as to what techniques should be used. A pragmatic approach to helping patients with particular problems is contrasted with general memory training and the assumptions underlying such training are discussed.
A clinical trial with desglycinamide arginine vasopressin for the treatment of memory disorders in man.
In a double-blind cross-over trial the memory effect of the neuropeptide desglycinamide arginine vasopressin (DGAVP) was selected because of its well-documented facilitatory effects on memory components in rodents. Patients with stabilized or progressive amnesic disorders (Korsakoff disease, early stages of Alzheimer dementia, head injuries and other central nervous system diseases) did not respond to the drug. Factors possibly explaining the discrepancy with animal research are discussed.
[Verbal memory disorders provoked by a variety of stokes].
In recent years a consensus has been reached about the neuroanatomical substrate of verbal memory, but this state of knowledge has not yet been implemented in clinical practice. One reason for this may be that most of the neuroscientific studies on verbal memory used different neuropsychological instruments and that only a small set of patient groups with the same etiology but different lesion sites were analysed. Returning to three earlier studies, we analyse the possibility to make differential judgements on the verbal memory impairments of four different patient groups by using the California Verbal Learning Test (CVLT). We compare patients with left-sided (n = 16) and right-sided (n = 10) posterior cerebral artery infarcts and patients with infarcts of the left (n = 10) or right (n = 21) frontal lobe, and we integrated data about their retention errors that had not been analysed so far. Our findings reveal significant differences between these patient groups, concerning the quantitative aspects of impairments, and also the profiles of memory errors (recall, interference and perseverations). Our study documents a relation between the site of the lesion and the type of verbal memory impairment, agreeing with some of the most recent neuroscientific findings. Starting from this observation we try to define a neuropsychological pattern of memory impairment which enables differential clinical diagnoses using the CVLT as a memory test.
The effect of Aricept in persons with persistent memory disorder following traumatic brain injury: a pilot study.
PRIMARY OBJECTIVE: To investigate the effectiveness of donepezil hydrochloride (Aricept) in treating persistent memory deficits in people with traumatic brain injury. RESEARCH DESIGN: Single subject ABAC design was used so that each participant could serve as their own control. METHODS AND PROCEDURES: Seven TBI survivors with persistent memory dysfunction, at least 1.5 years post-injury, underwent two 6-month trials of Aricept. The following tests were used to assess memory and cognition: Brief Visual Memory Test-Revised (BVMT-R), Hopkins Verbal Learning Test, Digit Span and Letter Number Sequence sub-test of the Wechsler Adult Intelligence Scale-III, Controlled Oral Word Association Test and Memory Functioning Questionnaire. EXPERIMENTAL INTERVENTION: During the first treatment phase, participants received 5 mg/day of Aricept for 1 month, increasing to 10 mg/day of Aricept for an additional 5 months. During the second treatment phase, participants received 5 mg/day of Aricept for the entire 6 months. MAIN OUTCOMES AND RESULTS: A repeated measures analysis of variance indicated significant improvement on immediate and delayed memory portions of the BVMT-R when taking 10 mg/day of Aricept. CONCLUSIONS: Findings contribute to the growing body of research into the use of Aricept in treating memory deficits in TBI survivors and support the need for further research.
The clinical management of HIV-related dementia and other memory disorders in the residential drug treatment environment.
Human immunodeficiency virus (HIV)-related dementia and other memory and attention disorders are described in terms of etiology, incidence, and symptoms. Assessment for cognitive impairment includes basic screening (examples are given), or a thorough neuropsychological evaluation. Implications for treatment within the residential drug treatment environment include: (a) providing accurate information to staff and residents; (b) identifying residents' anticipatory anxiety; (c) supportive counseling of residents; (d) coaching residents in the use of coping strategies; (e) creating environmental support; and (f) frequent reassessment of treatment goals, including the appropriateness of independent living. Helpful concrete suggestions are listed.
The coin-in-the-hand test: a new "bed-side" test for the detection of malingering in patients with suspected memory disorder.
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The short-term storage of auditory and visual two-channel digits by elderly patients with memory disorder.
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[Clinical approach to memory disorders].
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[Memory disorders and antitubercular therapy. A psychometric study].
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[Memory disorders following brain injuries].
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[Case of memory disorder treated with vasopressin].
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Clinical assessment of memory disorders in amnesia and dementia.
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Beneficial effects of DX-9386, a traditional Chinese prescription, on memory disorder produced by lesioning the amygdala in mice.
The amygdala is one of the key areas of the brain involved in learning and memory. Bilateral lesions of the amygdala in 9-week-old mice induced impairment of memory acquisition and retention. DX-9386, a traditional Chinese medicinal prescription consisting of ginseng, polygala, acorus and hoelen, was orally administered to the lesioned mice after the operation until all the experiments were completed. From 15d after surgery, learning behavior in the step-down test was observed daily for 10 d. DX-9386 treatment ameliorated the memory acquisition deficit. The number of step-down events in the first testing trial was significantly decreased by administration of 250 mg/kg of the prescription to the lesioned group of mice. Choline acetyltransferase activity in the cerebral cortex of the lesioned mice was significantly decreased, while repeated administration of the prescription did not affect this biochemical parameter. These results indicate that the memory acquisition enhancing effect of DX-9386 may not be achieved by direct activation of cholinergic transmission in the brain but by some other mechanism(s).