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 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Memory and attention were evaluated in 40 persons with a history of organic solvent exposure and 40 demographically similar controls. Exposed subjects, in comparison to controls, had reduced digit spans, were deficient at learning new information, and recall on a Brown-Peterson distractor test was especially low following a 30-sec interference interval. If original learning was considered, long-term recall was similar for both groups. On a test of sustained attention, the Continuous Performance Test, exposed subjects became less accurate over successive blocks, a pattern opposite to that seen in control subjects. The data suggest that the memory impairment following solvent exposure may result from deficient allocation of attentional resources due to the inability to deal effectively with an increase in processing load.
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PMID:Assessment of attention and memory efficiency in persons with solvent neurotoxicity. 143 37

Thirty-seven patients with multiple sclerosis (MS) were compared to 26 normal controls of equivalent age, education, and verbal intelligence on measures of verbal learning and memory (Digit Span and Supraspan, Brown-Peterson Distractor Task, Selective Reminding Test, Story Recall, and Free Verbal Recall) and verbal fluency (Letter and Animal Fluency). The MS patients exhibited deficits on measures of secondary (long-term) memory and verbal fluency, but performed normally on measures of primary (short-term) memory, recognition memory, and rate of forgetting from secondary memory. These results suggest that the memory disturbance in MS results primarily from an imparied ability to access information from secondary memory, while encoding and storage capacity is intact. Degree of memory impairment was unrelated to length of illness, severity of disability, or self-reported depression.
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PMID:On the nature of memory disturbance in multiple sclerosis. 280 59

This study reports the case of a 42-year-old man who suffered a ruptured aneurysm of the anterior communicating artery. His memory capabilities were assessed after a considerable recovery period during which many of his memory deficits ameliorated. His scan revealed a left frontal lesion and many of his deficits were characteristic of frontal impairment. He was impaired on temporal discrimination, and he showed marked source forgetting. He also performed badly on the Brown-Peterson task, and we suggest that this is another task that may be characteristic of frontal impairment. In contrast, the patient showed normal or near normal performance on some memory tasks but not on others. It is concluded that the patient's frontal signs are similar to those found in Korsakoff's Syndrome, but that his memory impairment is qualitatively different from that encountered in patients with the amnesic syndrome.
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PMID:Memory impairment following ruptured aneurysm of the anterior communicating artery. 337 1

Brain-derived neurotrophic factor (BDNF) has been suggested to be involved in memory processes. In the present study, the association between memory impairment at senescence and BDNF expression in the hippocampus was studied in 30-32-month-old Brown Norway rats, which had been maternally deprived early in life. These animals display a bimodal distribution in their spatial learning ability: rats are either non-impaired or impaired. BDNF mRNA expression in the hippocampus was compared between non-impaired and impaired rats. We measured BDNF mRNA expression in the hippocampus 3 h after training in the Morris water maze ('post-training') and at 1 month after training ('basal'). Non-impaired performers displayed a higher post-training BDNF mRNA level in the CA1 region than impaired rats. In addition, only in the non-impaired performers post-training BDNF mRNA levels in CA1 and dentate gyrus were increased as compared to basal levels. Thus, we have demonstrated that in senescent rats, hippocampal BDNF expression in response to water maze training is associated with memory performance.
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PMID:Correlation between hippocampal BDNF mRNA expression and memory performance in senescent rats. 1159 12

Semantic memory was evaluated in 124 epilepsy patients, including 84 with left (n=44) or right temporal lobe epilepsy (TLE) (n=40) and 40 with left (n=25) or right frontal lobe epilepsy (FLE) (n=15), in order to determine their verbal and visual deficits, and the neuroanatomical relationships between them. The controls were 35 healthy subjects. Semantic memory was assessed by means of Picture Naming, Picture Pointing, the verbal Pyramid and Palm Trees Test (PPTT), the visual PPTT, Object Decision Hard, and Drawing From Memory. Episodic memory was assessed by means of the Short Story, Rey's Complex Figure, the Verbal and Visual Selective Reminding Procedure and Brown-Peterson Procedure. Factor analysis of the epilepsy patients distinguished their semantic memory scores from other neuropsychological domains. The semantic memory factor was significantly related to the side of the epileptic region, with lower scores in the left hemisphere and left TLE patients. In comparison with the controls, the left TLE patients were significantly impaired on Picture Naming, Picture Pointing, and Object Decision Hard. Subsequent analyses showed that, in comparison with the controls and the right TLE patients, the left TLE patients with lateral temporal lobe lesions were impaired in Picture Naming whereas, in comparison with the controls, the left TLE patients with mesial temporal lobe lesions were impaired in Object Decision Hard. On the contrary, the episodic memory factor was not related to the side of the epileptic region, and a few material-specific tests revealed opposite impairments in the left and right hemisphere patients. These results show that left TLE may cause semantic memory deficits involving verbal and visual information. Unlike the material-specific pattern of episodic memory, this pattern of impairment is in line with the view of an amodal semantic store in which all of the information about a thing overlaps. The semantic memory impairment may reflect damage in the lateral and mesial temporal lobe regions that impair neocortical functions in storing and retrieving information or hippocampal functions in processing meaningful stimuli.
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PMID:Semantic memory in partial epilepsy: verbal and non-verbal deficits and neuroanatomical relationships. 1598 38

This paper reviews evidence from neuropsychological patient studies relevant to two questions concerning the functions of the medial temporal lobe in humans. The first is whether the hippocampus and the adjacent perirhinal cortex make different contributions to memory. Data are discussed from two patients with adult-onset bilateral hippocampal damage who show a sparing of item recognition relative to recall and certain types of associative recognition. It is argued that these data are consistent with Aggleton and Brown's (1999) proposal that familiarity-based recognition memory is not dependent on the hippocampus but is mediated by the perirhinal cortex and dorso-medial thalamic nucleus. The second question is whether the recognition memory deficit observed in medial temporal lobe amnesia can be explained by a deficit in perceptual processing and representation of objects rather than a deficit in memory per se. The finding that amnesics were impaired at recognizing, after short delays, patterns that they could successfully discriminate suggests that their memory impairment did not result from an object-processing deficit. The possibility remains, however, that the human perirhinal cortex plays a role in object processing, as well as in recognition memory, and data are presented that support this possibility.
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PMID:The role of the human medial temporal lobe in object recognition and object discrimination. 1619 72

Altered hippocampal synaptic plasticity may underlie age-related memory impairment. In acute hippocampal slices from aged (22-24 mo) and young adult (1-12 mo) male Brown Norway rats, extracellular excitatory postsynaptic field potentials were recorded in CA1 stratum radiatum evoked by Schaffer collateral stimulation. We used enhanced Ca(2+) to Mg(2+) ratio and paired-pulse stimulation protocol to induce maximum changes in the synaptic plasticity. Six episodes of theta-burst stimulation (TBS) or nine episodes of paired low-frequency stimulation (pLFS) were used to generate asymptotic long-term potentiation (LTP) and long-term depression (LTD), respectively. In addition, long-term depotentiation (LTdeP) or de-depression (LTdeD) from maximal LTP and LTD were examined using two episodes of pLFS or TBS. Multiple episodes of TBS or pLFS produced significant LTP or LTD in aged and young adult rats; this was not different between age groups. Moreover, there was no significant difference in the amount of LTdeP or LTdeD between aged and young adult rats. Our results show no age differences in the asymptotic magnitude of LTP or LTD, rate of synaptic modifications, development rates, reversal, or decay after postconditioning. Thus impairment of the basic synaptic mechanisms responsible for expression of these forms of plasticity is not likely to account for decline in memory function within this age range.
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PMID:Aging effects on the limits and stability of long-term synaptic potentiation and depression in rat hippocampal area CA1. 1755 51

Radiation therapy is used widely to treat primary and metastatic brain tumors, but also can lead to delayed neurological complications. Since maintenance of myelin integrity is important for cognitive function, the present study used a rat model that demonstrates spatial learning and memory impairment 12 months following fractionated whole-brain irradiation (WBI) at middle age to investigate WBI-induced myelin changes. In this model, 12-month Fischer 344 x Brown Norway rats received 9 fractions of 5 Gy delivered over 4.5 weeks (WBI rats); Sham-IR rats received anesthesia only. Twelve months later, the brains were collected and measures of white matter integrity were quantified. Qualitative observation did not reveal white matter necrosis one year post-WBI. In addition, the size of major forebrain commissures, the number of oligodendrocytes, the size and number of myelinated axons, and the thickness of myelin sheaths did not differ between the two groups. In summary, both the gross morphology and the structural integrity of myelin were preserved one year following fractionated WBI in a rodent model of radiation-induced cognitive impairment. Imaging studies with advanced techniques including diffusion tensor imaging may be required to elucidate the neurobiological changes associated with the cognitive impairment in this model.
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PMID:Maintenance of white matter integrity in a rat model of radiation-induced cognitive impairment. 1962 28

The hippocampus processes memory is an early target of aging-related biological and structural lesions, leading to memory decline. With absent neurodegeneration in the hippocampus, which identified in rodent model of normal aging the pathology underlying age-related memory impairment is not complete. The effective glial-vascular networks are the key for maintaining neuronal functions. The changes of glial cells and cerebral capillaries with age may contribute to memory decline. Thus we examined age associated changes in neurons, glial phenotypes and microvasculature in the hippocampus of aged rats with memory decline. Young adult (6 months) and aged (35 months) male rats (Fisher/Norway-Brown) were used. To evaluate memory, four days of acquisition phase of Morris water maze tasks were carried out in both age groups and followed by a probe trial 2 h after the acquisition. The brains were then collected for analysis using immunochemistry. The aged rats showed a delayed latency (p<0.001) and longer swimming path (p<0.001) to locate a hidden platform. They also spent less time in and made delayed and fewer entries into the correct quadrant during the probe trial. Without seen neuronal degeneration, the aged rats with memory impairments have displayed dopamine depletion, profound vascular and microglial degeneration with reduced vascular endothelial growth factor and elevated GFAP expression in the hippocampus. The data indicate the memory decline with age is associated with neuronal dysfunction, possibly due to impaired glial-vascular-neuronal networks, but not neuronal degeneration. Glial and vascular degeneration found in aged rats may represent early event of aging pathology prior to neuronal degeneration.
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PMID:Age-related memory decline is associated with vascular and microglial degeneration in aged rats. 2288 27

Past studies have suggested that OCD patients suffer memory impairment on tasks using complex stimuli that require memory for combined elements to be maintained, but not for more simplistic memory tests. We tested this with 42 OCD patients and 42 healthy controls performed a computerized situation awareness task. In addition, participants completed the Yale-Brown Obsessive Compulsive Scale (Y-BOCS) and Maudsley Obsessive-Compulsive Inventory (MOCI). The OCD patients had poorer accuracy in integration/comprehension and perception levels than controls. There were significant correlations between situational awareness scores (i.e., visuo-spatial monitoring and processing) and Y-BOCS obsession-compulsion and slowness and doubt scores of MOCI in OCD patients. In addition, there were also significant correlations between situational awareness and controlling, cleaning, slowness, rumination and total scores of MOCI in control group. Results indicated that (I) OCD patients have problems of perception, integration, and comprehension of complex visual perceptions; (II) situation awareness deficits associated with severity and prevalence of obsessions and compulsions.
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PMID:Situation awareness in obsessive-compulsive disorder. 2353 45


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