Proactive interference and facilitation as a function of amount of training and stress.
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Two experiments explored the possibility that lesions of avian hyperstriatum, which disrupt reversal learning, might have that effect through a potentiation of the influence of proactive interference. Neither experiment found any evidence to suggest excessive interference in hyperstriatal pigeons, from preceding training on a position (or color) discrimination, on retention of a color (or position) discrimination, and this was true both after a short (30 min) and after a long (6 or 7 day) retention interval. There was, however, evidence of a disturbance, not easily interpreted, in retention following the lesions. There was also convincing evidence, from both experiments, for the disruption by hyperstriatal lesions not only of reversal learning but also of tasks not involving reversals, a disruption that suggests a general tendency to perseverate in hyperstriatal birds.
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Task decomposition provides supplementary data that complement traditionally computed performance indexes of multi-trial list learning. Both traditional and decomposition approaches can be combined to permit a thorough assessment of multiple aspects of learning and memory in patients with memory impairment. We applied task decomposition to investigate the relative roles of acquisition and consolidation in mediating the multi-trial learning deficit in patients with Alzheimer's disease. This goal was accomplished by decomposing recall performance across the five study-and-test trials of the Rey Auditory Verbal Learning Tests into measures that presumably tap intertrial acquisition and intertrial consolidation. As compared to matched controls, patients diagnosed with mild Alzheimer's disease showed lower gained access across trials, indicating that Alzheimer's disease impairs the ability to produce a stable memory representation of new material in long-term memory. Additionally, patients with Alzheimer's disease manifested higher lost access, which suggests that deficient consolidation leading to rapid intertrial forgetting also contributes to their poor learning. We argue that analytically decomposing learning curves will help both in uncovering the cognitive processes that underlie disease-related learning deficits in persons with memory disorders and can help to characterize potential areas for remediation.
Over the past decade, memory impairments associated with retrosplenial damage have received increased attention among neuroscientists, although the exact role of the retrosplenial region in memory has not been clearly defined. Evidence from lesion studies and functional neuroimaging has implicated the retrosplenial region in verbal episodic memory, temporal ordering of information, and topographical memory. In addition, recent positron emission tomography studies have shown increased activation of the retrosplenial cortex during tasks involving both the encoding and retrieval of episodic information. The objective of this study was to define more clearly the nature of memory impairments observed in retrosplenial amnesia. A 47-year-old amnesic male with a left retrosplenial arteriovenous malformation was examined on neurocognitive tasks of automatic and directed encoding, temporal ordering of information, and remote memory. Despite normal performance on frontal cognitive tasks, intact memory for remote information, and a superior IQ, this individual exhibited a profound deficit in the encoding of information, evidenced by poor release from proactive interference, poor category clustering on word list recall, poor semantic encoding on a levels of processing task, and mild impairments in temporal ordering. These results imply that the retrosplenial region plays a role in the verbal encoding of information, which contributes to the profound verbal memory impairment reported in previous case studies of patients with retrosplenial damage.
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Free recall of word lists was investigated in a sample of 47 patients with dementia of the Alzheimer type (DAT) and 31 normal controls of equivalent age and education. Recall was divided into primary memory (PM) and secondary memory (SM) components based on the number of items intervening between presentation and recall. The findings were as follows: (1) the patients showed a greater deficit on the SM than on the PM measure; (2) there was little evidence of proactive interference in the patient group; (3) the PM and SM measures were independent in the controls but not in the patient group; and, (4) the size of patients' PM deficit increased linearly with increasing items between presentation and attempted recall. These results suggest that the memory disorder of DAT is partially the result of defective PM.
Patients with Huntington's disease (HD) were compared to normal controls of equivalent age and verbal intelligence on a set of verbal learning tasks. Although the HD patients showed the expected deficit in secondary (long-term) memory, their performance was otherwise comparable to that of the control groups. Primary (short-term) memory was normal, there was normal sensitivity to proactive interference, and the patients showed an advantage, albeit reduced, in recall of related compared to unrelated word lists. The findings suggest that mnemonic input is encoded semantically in HD though less efficiently than in unafflicted individuals, and that difficulty accessing information in semantic (knowledge-based) memory may be partially responsible for the memory disorder of HD.
Episodic (recall of passages) and semantic (letter and category fluency) memory tasks were administered to Alzheimer's Disease (early stages), Huntington's Disease (HD), and alcoholic Korsakoff patients matched for overall severity of dementia. Although all three patient groups were severely (and equally) impaired on memory for passages, only the Alzheimer and Korsakoff patients emitted numerous intrusion errors. On the fluency tasks, the performance of the mild Alzheimer patients was distinguishable from that of the other two patient groups. On both fluency tasks, the HD and Korsakoff patients demonstrated severe and moderate deficits, respectively, whereas the mild Alzheimer patients were impaired only on the category fluency task. As with the episodic memory test, the Alzheimer and Korsakoff patients made more perseverative errors than did the HD patients on letter fluency. These findings suggest that Alzheimer and HD patients' impairments on episodic and semantic memory tasks reflect different underlying processes. The performance of Alzheimer patients is affected by their language dysfunction and an increased sensitivity to proactive interference; the deficits of the HD patients appear due to a general retrieval problem. Similarities in the error patterns (i.e., perseveration errors) of Alzheimer and Korsakoff patients are discussed with regard to recent neuropathological findings.
California Verbal Learning Test (CVLT) performance was compared for 33 head-injured and 33 neurologically normal adult males. On learning trials, head-injured persons recalled fewer items than controls in general, though the percent of improvement between trials did not differ for these groups. Head-injured patients also demonstrated more intrusions and used semantic groupings less than did normal controls during learning trials. On delayed recall trials, head-injured persons remembered a smaller percentage of items they had learned earlier than did controls. Semantic cues aided recall for head-injured but not normal persons. Head-injured persons were less able to discriminate list from nonlist items during the recognition trial. Results indicated both retrieval and storage (i.e., encoding or retention) deficits for the head-injured group. The CVLT is a useful instrument for defining memory deficits in a head-injured population.
The role of proactive interference in verbal memory was examined in 154 normal and brain-damaged subjects. Subjects were matched on age, sex, education, presence or absence of brain damage, and administered the Wechsler Memory Scale (WMS) Stories in standard order (A+B) or reverse order (B+A). Both normal and brain-damaged subjects recalled fewer details from Story B than Story A regardless of order of administration. We conclude that Story B from the WMS is inherently a more difficult passage to recall than Story A. The recall of fewer Story B items relative to Story A is expected and not due to proactive interference.
Diencephalic and temporal amnesics display an excessive sensitivity to proactive interference (PI) in memory tasks of the AB/AC kind. There exists considerable controversy about the nature of this sensitivity to PI. Moreover, it is an open question whether such sensitivity to PI is an obligatory feature of amnesia, or rather an incidental result of frontal damage often reported in amnesics. This question was reexamined by enrolling patients with an operated aneurysm of the anterior communicating artery (ACoA) and matched controls for an AB/AC learning task of two lists of 12 paired-associate words. It appeared that ACoA patients, like diencephalic and temporal amnesics, did indeed display a marked sensitivity to PI when compared to normals (Exp. I), even when performance of both groups in the learning of the first list was equated (Exp. II). The distribution of errors made in learning the second list, as well as the correlations between performance in learning the second list and a Stroop test, suggest that sensitivity to PI in ACoA amnesics could be the consequence of an inability to suppress irrelevant information at retrieval due to defective inhibitory attentional mechanisms. Complementary data collected in a small sample of Korsakoff's amnesic subjects are also described.
Capacity limits in short-term recall were investigated using proactive interference (PI) from previous lists in a speeded-recognition task. PI was taken to indicate that the target list length surpassed working memory capacity. Unlike previous studies, words were presented either concurrently or sequentially and a new method was introduced to increase the amount of PI. On average, participants retrieved about four items without PI. We suggest an activation-based account of capacity limits.
We evaluated a 23 year-old man after recovery from encephalitis. In contrast to the expected pattern of increasingly better acquisition across the 5 learning trials of the California Verbal Learning Test (CVLT-2), he produced a "J-shaped" curve (Trials 1-5: 8,6,6,9,11). Because he also demonstrated excessive levels of proactive interference as well as poor divided attention, we hypothesized that his atypical learning pattern was due to a build-up of proactive interference secondary to executive dyscontrol. Using a large sample of 4462 healthy adult men, we identified four groups exhibiting various learning patterns. We found that a learning pattern similar to this patient (i.e., a drop after trial 1 followed by recovery) was rare (1.1% of the sample). Individuals with this learning pattern demonstrated increased perseverative responses, as well as greater difficulty maintaining cognitive set on the Wisconsin Card Sorting Test, decreased attentional control on the Paced Auditory Serial Addition Test, and greater levels of proactive interference on the CVLT. Taken together, the results of the study suggest that an early drop, followed by a recovery in learning trial performance, is associated with executive dyscontrol.
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In order to determine the effects of growth hormone (GH) on long term memory, two experiments were carried out, all involving a common paradigm. Mice were given massed training on a discrimination task and were injected with GH or control substances before and/or after training: retention was measured 4 weeks later. In Experiment 1, different groups of mice were injected with either GH or saline at five different time points relative to original learning (OL): 90, 30, and 5 min before, and 5 and 30 min after. The results showed a significant quadratic trend, in the form of a U-shaped curve for the GH-injected groups at retention. Maximal retention was observed at the 90 min pre-OL and the 30 min post-OL injection groups. Poorest retention was shown by the 5 min pre-OL injection group. In Experiment 2, GH, saline, and thyroid-stimulating hormone (TSH) were administered at 90 and 5 min pre-OL. In addition, a "state dependency" hypothesis was tested using additional groups of mice. The results again showed a severe drop in retention when GH was administered 5 min before OL; differences between the two pre-OL GH injection groups were less marked than in Experiment 1; TSH did not have the same action as GH; and finally, a state dependency interpretation was ruled out. Together the two experiments present results that indicate a selectively GH-induced suppression of memory when GH is administered in close proximity to OL. As the time lapse between the injection of drug and the learning task increases, the inhibitory effect on memory is reversed.
OBJECTIVES: To explore the contribution of executive dysfunctions to mnemonic problems in adults with mild traumatic brain injury (MTBI). DESIGN: Prospective quasiexperimental between-groups design. PARTICIPANTS: Ninety-nine persons with MTBI were compared to 90 control group participants matched for gender, age, and education. SETTING: Two Canadian brain injury rehabilitation programs. MAIN OUTCOME MEASURE: California Verbal Learning Test. RESULTS: Participants with MTBI showed a significant deficit in free recall on the California Verbal Learning Test but performed similarly to the comparison group on the recognition task. Furthermore, the participants with MTBI were less likely to use semantic clustering as a memorizing strategy and made more intrusion errors and false-positive errors on the recognition task. CONCLUSIONS: While the scores for the participants with MTBI are only slightly lower than the norm, they demonstrate that MTBI has a negative effect on mnemonic performance. The results are explained in terms of a deficit in registration/retrieval processes rather than a malfunction of the storage processes. This supports the initial hypothesis that executive dysfunctions are detrimental to the quality of mnemonic functions in patients with MTBI.
This study evaluated the hypothesis that schizophrenic conceptual disorder derives from abnormal verbal encoding, geared to salient affective and physical cues at the expense of conceptual attributes. Subjects were 63 adult psychotic inpatients, including 42 schizophrenics and 21 nonschizophrenics of similar age, sex, race, and chronicity. They underwent 12 trials on Wickens' release from proactive interference (PI) procedure to measure reliance on three dimensions for encoding: conceptual (taxonomic class), affective (Evaluation axis of the semantic differential), and physical (rhyming sounds). The release effect for schizophrenics, compared with controls, was found to be significantly weaker on the conceptual dimension and correspondingly stronger on the affective dimension. Whereas controls exhibited the normal attraction to conceptual over other cues, schizophrenics presented a flat profile. Nonparanoid and thought-disordered schizophrenics showed particular deficits on the conceptual dimension. All schizophrenic groups contrasted controls by their diminished PI release with less salient concepts. The results thus suggested that encoding by schizophrenics is uniquely oriented to stimulus salience rather than semantic relevance. A fundamental deficiency in processing of cues essential for conceptual operations, accordingly, seems to underlie the conceptual dysfunction in schizophrenia. The implications were discussed in relation to diversities in the cognitive literature and prevalent theories.