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Query: UMLS:C0751295 (memory loss)
 3,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nature of remote memory impairment in patients with medial temporal lobe damage is the subject of some debate. While some investigators have found that retrograde amnesia in such patients is temporally graded, with relative sparing of remote memories (Squire and Alvarez, 1995), others contend that impairment is of very long duration and that remote memories are not necessarily spared (Sanders and Warrington, 1971; Nadel and Moscovitch, 1997). In this study, remote memory was assessed in 25 patients with unilateral temporal lobe epilepsy and 22 non-neurologically impaired controls using the Autobiographical Memory Interview (Kopelman et al., 1989). Results indicate that patients have impaired personal episodic memory but intact personal semantic memory. The impairment extends even to the most remote time periods in early childhood, long before seizure onset in many patients. As well, patients awaiting temporal lobectomy for control of seizures perform as poorly as those who have already undergone resective surgery. These results support the hypothesis that temporal lobe damage or dysfunction, caused by recurrent seizures or surgical excision, results in extensive retrograde amnesia for personal episodic memories. Interestingly, patients with radiological evidence of hippocampal sclerosis were not significantly more impaired than those without obvious sclerosis. These results indicate that even minimal damage to medial temporal lobes results in significant impairment to autobiographical episodic memory. These findings are more compatible with a memory loss or retrieval deficit rather than a consolidation account of remote memory impairment.
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PMID:Remote episodic memory deficits in patients with unilateral temporal lobe epilepsy and excisions. 1090 28

This paper describes a 56 year old female patient (JJ) who suffered a minor head injury at work and presented with profound retrograde amnesia for both public events and autobiographical material spanning her entire life. In addition, she complained of word-finding difficulties and anterograde memory impairment and neuropsychological assessment found evidence of mild executive dysfunction. Neurological investigations (CT and EEG) were essentially normal although changes indicative of small vessel disease were noted on MRI brain scan. Various forms and aetiologies of remote memory loss were considered including, simulated, psychogenic and organic amnesia, but differential diagnosis proved difficult. It is proposed that criteria used in clinical practice to differentiate functional and organic complaints are limited and this may be because (1) both factors can be involved in the aetiology of amnesia, and (2) a similar underlying brain mechanism, such as a retrieval deficit could underlie many instances of organic and psychogenic amnesia. Future research, complemented by functional brain imaging, is needed to explore the nature of retrieval deficits.
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PMID:Profound retrograde amnesia following mild head injury: organic or functional? 1105 53

Adults with Down's syndrome (DS) are known to be at risk of dementia of the Alzheimer type (DAT), but because of their lifelong intellectual deficits, it is difficult to determine the earliest signs and characteristics of age-associated decline and dementia. In a longitudinal study in which all participants were healthy at the time of their entry into the study, the present authors compared the amount of decline on the subtests of the WISC-R to determine the sequence of cognitive decline associated with varying stages of dementia. Twenty-two individuals with varying degrees of cognitive decline were compared to 44 adults with DS who have remained healthy. All participants functioned in the mild or moderate range of intellectual disability at initial testing. On each subtest of the WISC-R, the amount of change experienced by the healthy participants over the study period was compared to the amount of change found for each of the groups with decline. Out of the individuals who showed declines, 10 adults with DS were classified as having 'questionable' decline based on the presence of memory impairment, and five and seven adults with DS were classified as in the 'early stage' and 'middle stage' of DAT, respectively, based on the presence of memory impairment, score on the Dementia Scale for Down Syndrome and a physician's diagnosis. It was found that participants who were identified as 'questionable', in addition to the memory loss that determined their classification, also showed significant declines on the Block Design and Coding subtests. The five adults in the early stage of dementia showed declines on these subtests, and in addition, on the Object Assembly, Picture Completion, Arithmetic and Comprehension subtests. The seven adults in the middle stage of dementia showed declines on these subtests, plus declines on Information, Vocabulary and Digit Span subtests. The Picture Arrangement and Similarities subtests were not useful in distinguishing between the groups because of baseline floor effects for a substantial proportion of participants. The present longitudinal study showed a sequence of cognitive decline associated with DAT, beginning with a possible 'pre-clinical' stage, and progressing through the early and middle stages. This approach begins to define the sequence of declining cognitive capacities that contributes to the observed functional deterioration caused by Alzheimer's disease and that is likely to reflect the involvement of cortical areas as the disease progresses.
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PMID:Sequence of cognitive decline in dementia in adults with Down's syndrome. 1111 20

Subjective memory complaint is common in later life. Its relationship to future risk of dementia is unclear, although many reports have found a positive association. We designed the present cross-sectional survey to investigate the clinical features associated with subjective memory impairment. One hundred and eight volunteers and 38 non-complainers acting as age-matched controls were recruited. Eleven subjects with memory complaints were excluded because of prior stroke or low MMSE score. The CAMCOG was used to measure cognition; complainers had significantly lower scores (p<0.001). Univariate analysis showed that complainers had greater prevalence of depression, anxiety, insomnia, psychotic phenomenon, difficulties with ADL and word-finding difficulties. The frequency distribution of the apolipoprotein E epsilon4 allele was similar for both groups (p=0.469). Logistic regression analysis indicated that CAMCOG scores (p=0.002) and word-finding difficulty (p=0.002) were independently associated with memory complaints. These results show that memory complainers have worse cognitive performance than non-complainers and support the findings of other studies that suggest that subjective memory loss may be a reliable indicator of cognitive decline.
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PMID:Clinical characteristics of individuals with subjective memory loss in Western Australia: results from a cross-sectional survey. 1124 22

Alzheimer's disease (AD) is a neurodegenerative condition, believed to be irreversible, characterized by inexorable deterioration of memory and intellect, with neuronal loss accompanying amyloid plaques and neurofibrillary tangles. In an amyloid precursor protein transgenic mouse model, Tg2576, little or no neuronal loss accompanies age-related memory impairment or the accumulation of Abeta, a 40-42 aa polypeptide found in plaques. Recently, we have shown inverse correlations between brain Abeta and memory in Tg2576 mice stratified by age (Westerman et al., 2002). Broadening the age range examined obscured this relationship, leading us to propose that small, soluble assemblies of Abeta disrupt cognitive function in these mice. Here we show that memory loss can be fully reversed in Tg2576 mice using intraperitoneally administered BAM-10, a monoclonal antibody recognizing the N terminus of Abeta. The beneficial effect of BAM-10 was not associated with a significant Abeta reduction, but instead eliminated the inverse relationship between brain Abeta and memory. We postulate that BAM-10 acts by neutralizing Abeta assemblies in the brain that impair cognitive function. Our results indicate that a substantial portion of memory loss in Tg2576 mice is not permanent. If these Abeta assemblies contribute significantly to memory loss in AD, then successfully targeting them might improve memory in some AD patients.
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PMID:Reversible memory loss in a mouse transgenic model of Alzheimer's disease. 1215 10

Severe amnesia in epileptic patients is a catastrophic condition that may be due to different etiologies. Because of the striking findings and thorough neuropsychological studies of Patient H.M., the literature has focused on postsurgical occurrence of such memory impairment, with much less emphasis on other causes. Here we summarize, for comparison, the history of H.M. We report five patients with pronounced memory loss who had extensive neuropsychological and electroencephalographic testing. MRI was also performed in four of the patients, MRI volumetric measurements of amygdala and hippocampal formation in three, and measurements of entorhinal cortex in two. The amnesia occurred after head trauma in one patient, following encephalitis in one, after partial status epilepticus in two, and after unilateral surgical resection in a woman with bilateral lesions. On the basis of these studies it was impossible to distinguish the role of recurrent temporal lobe epileptic seizures as distinct from underlying lesions in the genesis and course of the memory loss. We review here the anatomical substrate, neuropsychological, and other investigations and the etiological factors leading to the amnesia in these patients, together with current concepts regarding possible causes of such severe memory dysfunction. In patients with this degree of severity of memory deficit, temporal resection in an attempt to control seizures did not lead to a measurable increase in memory problems. It also, however, did not bring about worthwhile improvement in seizure control.
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PMID:Severe Amnesia in Epilepsy: Causes, Anatomopsychological Considerations, and Treatment. 1260 67

Chronic brain hypoperfusion (CBH) using permanent occlusion of both common carotid arteries in an aging rat model, has been shown to mimic human mild cognitive impairment (MCI), an acknowledged high risk condition that often converts to Alzheimer's disease. An aging rat model was used to determine whether hippocampal nitric oxide (NO) is abnormally expressed following CBH for two or eight weeks. At each time point, spatial memory was measured with the Morris water maze and hippocampal A beta 1-40/1-42 concentrations were obtained using sandwich ELISA. Real-time amperometric measures of NO representing the constitutive isoforms of neuronal nitric oxide synthase (nNOS) and endothelial (e)NOS were also taken at each time point to ascertain whether NO levels changed as a result of CBH, and if so, whether such NO changes preceded or followed any memory or amyloid-beta pathology. We found that two weeks after CBH, NO hippocampal levels were upregulated nearly four-fold when compared to nonoccluded rats but no alteration in spatial memory of A beta products were observed at this time point. By contrast, NO concentration had declined to control levels by eight weeks but spatial memory was found significantly impaired and A beta 1-40 (but not A beta 1-42) had increased in the CBH group when compared to control rats. Since changes in shear stress are known to upregulate eNOS but generally not nNOS, these results suggest that shear stress induced by CBH hyperactivated vascular NO derived from eNOS in the first two weeks as a reaction by the capillary endothelium to maintain homeostasis of local cerebral blood flow. The return of vascular NO to basal levels after eight weeks of CBH may have triggered metabolic changes within hippocampal cells resulting in hippocampal dysfunction as reflected by spatial memory impairment and by accumulation of A beta 1-40 peptide. In conclusion, our study shows that CBH initiates spatial memory loss in aging rats thus mimicking human MCI and also increases A beta 1-40 in the hippocampus. The memory and amyloid changes are preceded by NO upregulation in the hippocampus. These preliminary findings may be important in understanding, at least in part, the molecular mechanisms that precede memory impairment during chronic brain ischemia and as such, the pre-clinical stage leading to Alzheimer's disease.
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PMID:Hippocampal nitric oxide upregulation precedes memory loss and A beta 1-40 accumulation after chronic brain hypoperfusion in rats. 1450 18

This investigation evaluates effects of care consultation delivered within a partnership between a managed health care system and Alzheimer's Association chapter. Care consultation is a multi-component telephone intervention in which Association staff work with patients and caregivers to identify personal strengths and resources within the family, health plan, and community. The primary hypothesis is that care consultation will decrease utilization of managed care services and improve psychosocial outcomes. A secondary modifying-effects hypothesis posits benefits will be greater for patients with more severe memory impairment. The sample is composed of managed care patients whose medical records indicate a diagnosis of dementia or memory loss. Patients were randomly assigned to an intervention group, which was offered care consultation in addition to usual managed care services, or to a control group, which was offered only usual managed care services. Data come from two in-person interviews with patients, and medical and administrative records. Results supporting the primary hypothesis show intervention group patients feel less embarrassed and isolated because of their memory problems and report less difficulty coping. Findings consistent with the modifying-effects hypothesis show intervention group patients with more severe impairment have fewer physician visits, are less likely to have an emergency department visit or hospital admission, are more satisfied with managed care services, and have decreased depression and strain.
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PMID:Outcomes for patients with dementia from the Cleveland Alzheimer's Managed Care Demonstration. 1469 Aug 67

A number of theories posit a relationship between autobiographical memory and identity. To test this we assessed the status of autobiographical memory and identity in 20 individuals with Alzheimer's disease (AD) and 20 age-matched controls, and investigated whether degree of autobiographical memory impairment was associated with changes in identity. Two tests of autobiographical memory (Autobiographical Memory Interview, autobiographical fluency) and two measures of identity (Twenty Statements Test, identity items of the Tennessee Self Concept Scale) were administered. AD participants exhibited significant impairments on both memory tests, and changes in the strength, quality, and direction of identity relative to controls. Impairments of some components of autobiographical memory, particularly autobiographical memory for childhood and early adulthood, were related to changes in the strength and quality of identity. These findings support the critical role of early adulthood autobiographical memories (16-25 years) in identity, and suggest autobiographical memory loss affects identity.
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PMID:Memory of myself: autobiographical memory and identity in Alzheimer's disease. 1509 21

We estimated the relative frequency of isolated memory impairment versus isolated and comorbid impairment in executive control function (ECF). One hundred and ninety-three noninstitutionalized residents of a single Comprehensive Care Retirement Community (mean age 79.2 years) were investigated. The subjects were tested with multiple measures of memory and ECF. Test scores were standardized to minimize scaling effects. 'Impairment' was defined as performance < or =1.5 standard deviations below the mean for the entire sample (i.e., a z score < or =-1.5). Disability was estimated as the sum of self-reported activities of daily living and instrumental activities of daily living. The cognitive test performance was significantly associated with functional impairment, independently of age. ECF and memory measures were significantly intercorrelated. Both were significantly and independently associated with disability ratings. 6-10% of the subjects had memory impairment; 25-35% of the memory-impaired subjects had comorbid ECF impairments. An additional 4-7% of the subjects had isolated ECF impairment. A significant fraction of the cases otherwise meeting the criteria for 'mild cognitive impairment' may have comorbid ECF impairment. This raises the issue of whether they might be more properly classified as 'demented'. In addition, isolated ECF impairment may affect almost as many persons as isolated memory impairment. Isolated ECF impairment is not consistent with the natural history of preclinical Alzheimer's disease, suggests other conditions, and can be disabling, independently of age and/or memory loss.
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PMID:Misclassification is likely in the assessment of mild cognitive impairment. 1527 21


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