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Andrew R Mayes

Publications and source records attributed to Andrew R Mayes.

9 recordsLinked to original sources

The neural system that mediates familiarity memory.

In recognition memory tests, feelings of familiarity for stimuli vary in strength. Increasing levels of felt familiarity should modulate activity in brain structures that mediate familiarity memory. We used this expectation to identify the neural system that underlies scene familiarity memory. Normal subjects studied pictures of scenes and 2 days later while undergoing event-related functional magnetic resonance imaging (fMRI) rated old and new pictures as novel, slightly familiar, moderately familiar, very familiar, or recollected, although they were specifically instructed not to try and recollect. Familiarity strength was, therefore, judged as absent (misses) or present at three levels of increasing strength. A parametric analysis showed that, as perceived strength of familiarity increased activity in the perirhinal cortex, insula and left superior temporal cortex declined linearly whereas activity in the left dorsomedial thalamus, left ventrolateral and anteromedial frontal cortex, posterior cingulate cortex, and left parietal neocortex increased linearly. Hippocampal activity was not modulated linearly or quadratically by changes in familiarity strength. Recollection activated the hippocampus, and left anterior and inferolateral frontal and parietal cortices more than strong familiarity. In contrast, no brain region that was unaffected by recollection (relative to misses and correct rejections) was modulated by variations in familiarity strength. The implications of these findings for the functional and neural bases of familiarity and recollection are considered.

Adult↗

When memory does not fail: familiarity-based recognition in mild cognitive impairment and Alzheimer's disease.

Recognition can be guided by familiarity, a restricted form of retrieval devoid of contextual recall, or by recollection, which occurs when retrieval is sufficient to support the full experience of remembering an episode. Recollection and familiarity were disentangled by testing recognition memory using silhouette object drawings, high target-foil resemblance, and both yes-no and forced-choice procedures. Theoretically, forced-choice recognition could be mediated by familiarity alone. Alzheimer's disease and its preclinical stage, mild cognitive impairment (MCI), were associated with memory impairments that were greater on the yes-no test. Remarkably, forced-choice recognition was unequivocally normal in patients with MCI compared with age-matched controls. Neuropathology in hippocampus and entorhinal cortex, known to be present in MCI, presumably disrupted recollection while leaving familiarity-based recognition intact.

Aged↗

Sparing of the familiarity component of recognition memory in a patient with hippocampal pathology.

Subject KN has a persistent anterograde amnesia as a result of brain injury following meningitis in 1993. MRI scans reveal a bilateral decrease in the volume of his hippocampal region (dentate gyrus, CA1-4, subicular cortices) of approximately 45% in both the right and left hemispheres, although the volume of his perirhinal cortex appears normal. Aside from some changes to his occipital lobe and bilateral shrinkage of the amygdala, the rest of his brain appears normal on recent quantitative MRI scans. A striking feature of his memory loss is his ability to perform at normal levels on some tests of recognition, despite his consistent deficit on tests of recall. Two tests designed specifically to distinguish performance of two putative divisions of recognition memory (the Remember/Know procedure and the use of receiver operating characteristics to distinguish familiarity and recollection), provide evidence for a selective sparing of the familiarity component of recognition. The dissociation within recognition memory supports dual-process models of recognition, and also supports proposals that anatomically linked regions within the medial temporal lobe make qualitatively different contributions to recognition.

Adult↗

Long-term spatial memory: introduction and guide to the special section.

This article provides an introduction to the Special Section on Long-Term Spatial Memory in the journal Neuropsychology. It defines long-term spatial memory, explores how it has been considered historically, and provides brief descriptions of the principle cognitive mechanisms, with a guide to the terminology used in this field.

Animals↗

Recalling spatial information as a component of recently and remotely acquired episodic or semantic memories: an fMRI study.

Activations produced by the recall of episodic and semantic memories differing in spatial content and age were examined. Recall of recent episodic memories with differing spatial content activated the medial temporal lobes and the retrosplenial-posterior cingulate cortex-precuneus complex more than recall of recent semantic memories with similarly differing spatial content. Some of these differences related to the amount of spatial information recalled because spatially richer recent memories, regardless of whether they were episodic or semantic, activated the right posterior parahippocampal cortex, precuneus, and posterior parietal cortex more. This spatial effect was found to be independent of memory age for semantic memories, although some episodic-semantic memory differences, including one in the left hippocampus, were not age independent. Episodic-semantic memory recall activation differences are therefore probably a function of the amount recalled, memory age, and what is recalled, particularly with respect to spatial information.

Adult↗

Temporal order memory in patients with Korsakoff's syndrome and medial temporal amnesia.

Two groups of patients with global amnesia resulting either from Korsakoff's syndrome (KS) or from medial temporal lobe (MTL) damage were compared with groups of matched healthy control subjects on a list discrimination paradigm. Item recognition memory was matched across the amnesic and control groups in order to determine whether KS, but not MTL amnesics are disproportionately impaired on list discrimination as predicted by Parkin's [Functional significance of etiological factors in human amnesia. In: Squire LR, Butters N, editors. Neuropsychology of memory, 2nd ed. New York: The Guilford Press, 1992] hypothesis. However, both patient groups were impaired disproportionately on the temporal order memory task, which is inconsistent with Parkin's hypothesis. It remains possible that the KS patients are more disproportionately impaired than those with MTL damage because both patient groups performed at floor on the list discrimination task. The results are consistent with theories that postulate a critical role for the hippocampus in the kind of associative memory which underlies memory for temporal order, but not in recognition of single items or arbitrary associations between items of similar kinds.

Adolescent↗

Novelty-related activation within the medial temporal lobes.

Functional magnetic resonance imaging (fMRI) was used to examine whether (1) verbal associative encoding activates the medial temporal lobes (MTL) and related regions more than non-associative encoding, (2) verbal associative novelty is related to enhanced MTL activation, and (3) verbal item novelty is related to enhanced MTL activation and, if so, whether these activations are in different or overlapping sites. No increase in MTL activation was found during verbal associative encoding relative to non-associative encoding, although associative encoding was related to a relative increase in activation in the posterior cingulate cortex. In contrast, verbal associative novelty was found to activate the MTL and posterior cingulate cortex. Verbal item novelty did not significantly activate any brain region. The verbal associative novelty-related effect occurred despite subjects having little awareness of associative novelty. The verbal associative novelty-related activation in the MTL may be related either to unconscious novelty detection or to a priming effect at encoding. We argue that if the priming explanation is correct then this may account for our failure to observe an associative encoding MTL activation.

Adult↗

Long-term amnesia: a review and detailed illustrative case study.

Long-term amnesia is a slowly developing form of anterograde amnesia accompanied by retrograde amnesia of variable severity (Kapur, 1996; 1997) often associated with damage to the anterior temporal neocortex and epileptic seizures. The precise neural and functional deficits that underlie this condition are unknown. A patient, JL, who has this condition following a closed-head injury, is described in detail. Her injury caused bilateral anterior temporal neocortex damage that was more extensive on the left and right-sided damage to the perirhinal and orbitofrontal cortices. The hippocampus appeared to be intact bilaterally. Epilepsy developed within two years of JL's injury. Apart from her memory impairments, JL's cognitive functions, including high-level visual perception, attention, semantic memory and executive functions were well preserved. Her memory also seemed well preserved for at least 30 minutes following encoding. The one exception was the patient's relatively greater impairment at difficult visual recognition tests for which verbalization may not have been an effective strategy. This problem may have been caused by JL's right-sided perirhinal and orbitofrontal cortex damage. Her recall and recognition was clearly impaired after a three-week delay. She also showed a retrograde amnesia, which appeared to be milder than her remote post-morbid memory deficit. JL's remote memory was preserved for information first encountered in either the pre- or post-morbid period provided the information had received sufficient rehearsal over long periods of time. Her long-term amnesia may have been caused by anterior temporal neocortex damage, possibly in association with her epileptic seizures. Whether the condition is heterogeneous, involves a deficit in slow consolidation, disruption of unconsolidated memories, or blockage of maintenance or disruption of insufficiently rehearsed memories whether or not these have been slowly consolidated is discussed.

Adult↗