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The contribution of the thalamus to the functioning of prospective memory (PM) is currently unknown. Here we report an experimental investigation of the performance of two patients with bilateral infarcts in the anterior-mesial regions of the thalami on an event-based PM paradigm. One patient, G.P., had a pervasive declarative memory impairment but no significant executive deficit. The other patient, R.F., had a memory deficit limited to verbal material with associated behavioral abnormalities (inertia and apathy); she performed poorly on tests of executive functions. Although both patients performed poorly on the PM task, a qualitative analysis of performance revealed different mechanisms at the base of their impaired PM. G.P. had reduced declarative memory for target words compared with normal controls; but, unforgotten words were normally able to elicit his recall of the prospective intention. Conversely, R.F.'s declarative memory for target words was as accurate as that of normal controls, but she presented a dramatically reduced ratio between the number of target words she recalled and the number of times she activated the prospective intention on the PM task, suggesting that her deficit consisted of difficulty in activating the intention despite normal declarative memory for the target events. In conclusion, results of the present study demonstrate that thalamic structures have an important role in PM processes. They also document that damage to the anterior-mesial regions of the thalami affects PM abilities by two different mechanisms, respectively based on the relative disruption of declarative memory or executive processes functioning, which, in turn, is related to the specific intrathalamic structures involved by the lesions. Indeed, while G.P.'s pervasive declarative memory deficit was underlain by bilateral involvement of the mammillo-thalamic tract, R.F.'s executive and behavioral abnormalities were likely related to bilateral damage of the midline, intralaminar, and medio-dorsal nuclei., (Copyright © 2010 Elsevier Ltd. All rights reserved.)

A deficit of declarative memory is a common sequela after a hypoxic episode. While the role of gray matter changes (i.e., atrophy of hippocampal formation) as mainly responsible for memory loss has been emphasized, the role of the white matter damage has so far been neglected. The present study was aimed at evaluating whether white matter damage, within the neural circuitry responsible for declarative memory functioning, is present in anoxic patients. We assessed, by means of voxel-based morphometry, the integrity of white matter regions in five patients with hypoxic amnesia. When anoxic patients were compared to healthy controls, significantly less white matter density was detected in the fornix, anterior portion of the cingulum bundle and uncinate fasciculus bilaterally. We conclude that cerebral hypoxia may alter, together with the hippocampi, the integrity of white matter fibers throughout the memory-limbic system.

Anoxia is considered a good model for studying amnesia. However, not all individuals who experience anoxic events develop memory problems. Moreover, the question still remains about whether, after anoxia, damage is limited to the hippocampus in patients with amnesia and without other significant cognitive deficits. Here we investigated brain damage in a selected sample of adults affected exclusively by an amnesic syndrome after an anoxic episode. The cerebral MR images of these patients were submitted to visual inspection, volumetric measurements of the mesial temporal structures following manual segmentation, and to Voxel-Based Morphometry of the whole brain. We studied five anoxic patients and thirty-three well-matched healthy subjects. Our aim was to: (a) quantify regional atrophic changes associated with chronic anoxic damage compared to control subjects (Group Comparison Analysis); (b) identify regions of common abnormality across all patients (Conjunction Analysis in the VBM); (c) investigate whether measures of regional volume reduction correlated with neuropsychological memory scores; (d) compare the results obtained with visual inspection and ROI analyses with those obtained with VBM. We found that anoxic patients presented a significant reduction of gray matter volume in the hippocampus bilaterally compared to healthy subjects. The only common atrophic region across all patients was the hippocampus bilaterally. Correlation analysis showed only a trend between the Prose immediate free recall test and the left hippocampus. Our findings confirm that the hippocampus is very sensitive to damage stemming from anoxia. Patients with hypoxic amnesia may present damage in other brain regions, but only hippocampal atrophy is common in all of them.

Focal damage confined to the hippocampus may result in recognition deficits characterized by a dissociation between impaired recollection and preserved familiarity. Here, we report a single case of an amnesic patient with bilateral damage to the anterior part of the thalamus, who presented with a neuropsychological profile suggesting such a dissociation. We hypothesized that this focal damage involved the so-called Delay and Brion's circuit, which has been theorized to subserve episodic memory processes, but at a different anatomical level than in patients with hippocampal lesions. Using two independent experimental paradigms (remember/know and confidence receiver operating characteristics [ROC]) and recruiting a sex- and age-matched group of healthy controls, we demonstrated that this patient's recognition deficits were due to a selective impairment of recollection with a normal familiarity process. The patient underwent an ad hoc brain MRI study, and a quantitative analysis of his MR images was performed. Tissue damage extended bilaterally to the mammillo-thalamic tract, with complete preservation of the medio-dorsal thalamic nuclei. Our findings support the idea that the same functional specialization hypothesized for the different sub-regions of the mesial temporal lobe might also extend to the thalamus. This case will be discussed in light of its implications in support of recent theories, which regard recollection and familiarity as independent processes associated with different neural circuits.

Background: Different rates and cognitive predictors of conversion to dementia have been reported in subjects with different kinds of mild cognitive impairment (MCI)., Methods: A prospective, 24-month follow-up study, involving 269 subjects who strictly fulfilled criteria for the amnestic MCI., Results: Conversion rate to dementia was 21.4% per year. Seventy-nine out of the 83 individuals who developed dementia were affected by probable Alzheimer's disease (AD). Among others, at the 24-month follow-up 24.1% were still affected by amnestic MCI, 13.3% had changed their neuropsychological profile of impairment and 17.2% were cognitively normalised. Compared to subjects who did not convert to AD, those who did convert showed poorer immediate and delayed recall and recognition of verbal and visual material at baseline as well as reduced executive abilities. A combination of age, Clinical Dementia Rating boxes and scores on delayed recall and recognition of verbal and visual material accurately identified 86% of the subjects who developed AD., Conclusions: Elderly subjects affected by an isolated memory disorder have a high probability of developing AD. The ability of verbal and visual measures to predict incipient dementia of memory impairment may be increased by the simultaneous assessment of individual features, such as age or rate of functional impairment., (Copyright 2007 S. Karger AG, Basel.)

Different aspects of episodic long-term, short-term and implicit long-term memory were investigated in subjects who strictly fulfilled the criteria for the amnestic form of Mild Cognitive Impairment (a-MCI). Results showed normal short-term memory abilities in these subjects, while each of the episodic long-term memory indices explored showed poorer results in a-MCI subjects with respect to normal controls. Although some episodic memory functions were relatively well preserved, others appeared to have deteriorated to a level comparable to that of mild AD patients. The finding of an extensive impairment of all memory functions depending on hippocampal structures in a population with a high risk of developing dementia is strongly supportive of the hypothesis that a pure amnesic syndrome characterizes the preclinical phase of AD.

Ten amnesic patients of various etiologies and 10 matched normal controls participated in this study. On 2 consecutive days, subjects studied 30 novel word-word associations 6 times. Using a cued recall task, we assessed episodic learning and delayed retention of the study material immediately after each study phase and again 24 hr after the final study phase. Further, we evaluated implicit memory for new between-word associations by means of an automatic relational priming paradigm immediately after the delayed cued recall trial. Amnesic patients performed poorly on the cued recall task. Moreover, in the overall group of amnesics the priming effect failed to reach statistical significance. When the overall group of amnesics was split according to mean performance on the cued recall task, those in the low performer subgroup--comprised of 6 patients with direct or indirect involvement of the hippocampi--were particularly poor at episodically remembering the associations and did not reveal any relational priming. These data support the hypothesis of similar impairment of new episodic and implicit learning in amnesic patients and suggest that the hippocampus is crucial for both kinds of new learning.

Objective: To test the hypothesis that visual memory for faces can be dissociated from visual memory for topographical material., Method: A patient who developed a global amnesic syndrome after acute carbon monoxide poisoning is described. A neuroradiological examination documented severe bilateral atrophy of the hippocampi., Results: Despite a severe anterograde memory disorder involving verbal information, abstract figures, concrete objects, topographical scenes, and spatial information, the patient was still able to learn previously unknown human faces at a normal (and, in some cases, at a higher) rate., Conclusions: Together with previous neuropsychological evidence documenting selective sparing of topographical learning in otherwise amnesic patients, this case is indicative of the fact that the neural circuits involved in face recognition are distinct from those involved in the recognition of other visuoperceptual material (for example, topographical scenes).

This study was aimed at investigating functional and neuropsychological dissociations between repetition priming and explicit memory tasks. The explicit and implicit versions of the stem completion task were administered to a group of amnesics and a group of control subjects. In Experiment 1 both the explicit and implicit stem completions were significantly higher when the same presentation modality was used for studying and testing than when a change in modality from studying to testing occurred. Amnesics had normal implicit and deficient explicit completion performance. Experiment 2 revealed an advantage of the semantic over the phonological condition only in the explicit task and only in control subjects. Amnesic patients completed the same percentage of words as normal subjects in the phonological and semantic conditions of the implicit task and in the phonological condition of the explicit task but were deficient in intentionally completing semantically processed words. Possible interpretations of these results are discussed according to theoretical models that distinguish memory tasks along an explicit-implicit dichotomy (multiple memory system theory) or along a perceptual-conceptual dichotomy (transfer-appropriate procedures approach), and alternative theoretical positions are evaluated regarding repetition priming and memory deficits in amnesic patients.

This study was devised to investigate immediate and delayed recency effects in anterograde amnesic patients. For this purpose, a word-list immediate recall paradigm and a modified version of the procedure devised by Baddeley and Hitch [Attention and Performance, Erlbaum, NJ, 1977] for eliciting the recency effect in delayed recall conditions was administered to a sample of amnesic patients and to a group of age-matched healthy subjects. Amnesics disclosed a fully normal recency effect in the immediate recall paradigm and a deficient recency effect in the delayed recall condition. These data, taken together with experimental evidence from a patient affected by a pure form of phonological short-term memory impairment [35], draw a double neuropsychological dissociation suggesting a differential origin for the two kinds of recency effects: a short-term memory output underlying enhanced recall of terminal items in immediate recall paradigms, and an ordinal retrieval strategy applied to long-term memory stored units at the root of the delayed recency effect.

This study investigated the contribution of different components of the serial position curve to the accelerated forgetting rate displayed by amnesic and degenerative demented patients in word-list recall. For this purpose, we analyzed immediate and 15 min delayed recall performances on Rey's 15-word learning task of 16 pure amnesic, 15 Alzheimer's demented and 81 healthy subjects. Results documented that in all groups most forgetting occurred at the expense of terminal items of the word list. Nevertheless, both amnesic and demented patients showed a disproportionately larger memory loss on the recent part of the serial position curve than healthy subjects. Finally, amnesics (but not AD patients) suffered from a significantly larger forgetting rate for primacy items than normal controls. These data demonstrate that a critical deficit in memory disordered patients is represented by a failure in transferring information from a transitory memory status to a more durable storing condition. At least in amnesic patients, our results also suggest "true" long-term forgetting, presumably due to decay or to the intervening inaccessibility of previously stored memory representations.

This study investigated the hypothesis that memory disordered patients suffer of an exalted forgetting rate from long-term memory within the first few minutes following acquisition. For this purpose, we administered to groups of Alzheimer's (AD), Multi-infarct demented (MID), pure amnesic and age-matched normal controls a test involving immediate and 15-min delayed word-list recall and a modified version of the Huppert and Piercy's procedure (1978) assessing yes/no Recognition for pictures at 90 sec, 10 min, 1 hr and 24 hr delay intervals. Results showed an abnormal immediate/delayed performance decline for the word-list recall in AD and pure amnesic patients. In the same period, however, their Recognition score in the Huppert and Piercy's procedure decayed at normal rate. In the following intervals (1 hr and 24 hr), both groups disclosed abnormal forgetting slopes. Vascular demented patients, by contrast, disclosed fully normal forgetting rates both on the word-list recall and on the Huppert and Piercy's procedure. These findings are discussed in the light of cognitive mechanisms and neuroanatomical structures presumably underlying memory consolidation.

This study investigated the contribution of perceptual and conceptual processes to the repetition priming effect, and evaluated alternative theoretical positions about repetition priming in amnesic patients. Toward this end, we administered three repetition priming tasks (Stem Completion, Word Identification and Free Association) and an explicit memory task (yes/no Recognition) to amnesic and alcoholic patients, and tested the sensitivity of these tasks to level of processing and to manipulations of presentation modality. Experiment 1 demonstrated that the level of priming in Stem Completion and Free Association (but not in Word Identification) was enhanced by semantic elaboration of the stimuli. Experiment 2 revealed that the magnitude of priming in Word Identification and Stem Completion (but not in Free Association) was larger in the intramodal then in the intermodal condition. Amnesic patients displayed normal perceptual as well conceptual priming. Possible interpretations of these results according to theoretical models that distinguish memory tasks along an explicit-implicit dichotomy (multiple memory system theory), or on the basis of the extent to which they depend upon perceptual or conceptual processing (transfer-appropriate procedures approach), or that assumes a possible contamination of priming performance by explicit strategies of retrieval are discussed.

Despite considerable experimental work on Alzheimer's disease (AD), the underlying cognitive mechanisms as well as the precise localization of neuropathological changes critical for memory loss remains undefined. A review of the neuropsychological literature on long-term memory deficits in AD patients suggests that AD patients display (a) a pervasive deficit of explicit memory, (b) a partial deficiency of implicit memory for verbal and visuoperceptual material (as measured by repetition priming procedures), and (c) a substantial sparing of implicit memory for visuomotor skills. The explicit memory loss is likely a result of encoding as well as consolidation difficulties. A faulty lexical-semantic knowledge structure appears responsible for deficient repetition priming effects. Since neuropathological changes diffusely affect the brain of AD patients, establishing a clear relationship between localization of cerebral lesions and memory deficits is particularly difficult. Nevertheless, data suggest that extensive involvement of the hippocampal-amygdala complex plays a major role in explicit memory loss. Damage to associative cortical areas likely is involved in repetition priming deficits. The relative integrity of primary motor and sensory cortical areas and of the basal ganglia likely subsume, by contrast, the normal learning of visuomotor skills.