Memory Impairment in Out-of-Hospital Cardiac Arrest Survivors Is Associated With Global Reduction in Brain Volume, Not Focal Hippocampal Injury

Grubb, Neil R.; Fox, Keith A.A.; Smith, Kathryn H.; Best, J. J. K.; Blane, Annette; Ebmeier, Klaus P.; Glabus, Michael F.; O’Carroll, Ronan E.

doi:10.1161/01.str.31.7.1509

Cited by 111 publications

(72 citation statements)

References 28 publications

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“…However, the presumption of selective hippocampal damage in the absence of radiologic or histological data is unwarranted. Thus, in one study (Grubb et al, 2000), an MRI analysis of the brains of cardiac arrest survivors with evidence of memory impairment revealed global cerebral atrophy, rather than selective hippocampal damage. Whether or not the same is true of the patients tested by Yonelinas et al (2002) is not known.…”

Section: Resultsmentioning

confidence: 98%

Recall and recognition are equally impaired in patients with selective hippocampal damage

Wixted

Squire

2004

Cognitive, Affective, & Behavioral Neuroscience

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In two recent studies, the hypothesis that recall is more severely impaired than recognition in patients with damage thought to be limited to the hippocampus was tested. Yonelinas et al. (2002) reported findings that appeared to support this hypothesis, whereas Manns, Hopkins, Reed, Kitchener, and Squire (2003) found that recall and recognition were equally impaired. An analysis of the individual subject data from the two studies revealed that the apparent disagreement stemmed from the inclusion of a single outlying recognition score for 1 of the 55 control subjects in Yonelinas et al. (2002). When that outlier was excluded, the studies were in agreement that recognition and recall are substantially and similarly impaired in these patients. Yonelinas et al. (2002) also analyzed remember/know judgments and ROC data in an effort to show that recollection is selectively impaired in patients, but these analyses also raise problems.

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Section: Resultsmentioning

confidence: 98%

Recall and recognition are equally impaired in patients with selective hippocampal damage

Wixted

Squire

2004

Cognitive, Affective, & Behavioral Neuroscience

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“…The morphological and imaging data on cardiac arrest patients are scarce [2, 12,34,76,91]. Arbaelez et al published MRI findings in a series of patients with global cerebral hypoperfusion following cardiac arrest [2].…”

Section: Global Cerebral Ischemiamentioning

confidence: 99%

Lesion evolution in cerebral ischemia

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Hemmen

Schüler

2004

Journal of Neurology

104

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There is sound evidence from histopathological and magnetic resonance imaging (MRI) studies that focal ischemic brain lesions tend to increase in size over time. Considerable lesion growth was observed in models of animal stroke as well as in patients presenting with hemispheric stroke. In focal cerebral ischemia, lesions predominantly enlarge early within 12 hours after onset. Ischemic injury is caused by complete necrosis in most of the affected tissue. By contrast, in global cerebral ischemia as seen after cardiac arrest, lesions appear late (>12 h) in selectively vulnerable brain regions such as the hippocampus, and neurons are damaged by apoptotic cell death. The high and regionally distinct vulnerability of the brain explains why prolonged periods of global ischemia result in widespread loss of energy metabolites combined with diffuse brain edema and global damage. Postulated mechanisms involved in lesion growth include among others excitotoxicity, periinfarct depolarizations, lactacidosis, microcirculatory disturbances, and flow-metabolism uncoupling. Research in the field faces two main challenges. First,maturation phenomena of injury may require special imaging techniques to detect early ischemic changes. Second, the dynamic nature of the changes underlines the need to conduct longitudinal studies with a variety of imaging techniques (e. g., metabolic imaging, diffusion/perfusion MRI, positron emission tomography) that require a differentiated interpretation of the alterations observed.

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“…Some of these memory-impaired patients may have had damage limited to the hippocampus, but the idea that they all did is not a safe assumption. According to Grubb et al (2000),…”

Section: Patient Populationsmentioning

confidence: 99%

Recall, recognition, and the hippocampus: Reply to Yonelinas et al. (2004)

Wixted

Squire

2004

Cognitive, Affective, & Behavioral Neuroscience

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Two recent studies disagree about whether recall is more impaired than recognition (and recollection more than familiarity) in patients with damage limited to the hippocampus (Manns, Hopkins, Reed, Kitchener, & Squire, 2003;Yonelinas et al., 2002). Wixted and Squire (2004) pointed out that the disagreement about recall and recognition stems entirely from an outlying recognition score obtained by 1 of 55 control subjects in Yonelinas et al. (2002). In their comment on our paper, Yonelinas et al. (2004) minimize the importance of this result and argue that the role of the hippocampus in recollection and familiarity is best studied using different methods that attempt to measure these processes directly. Here, we argue that the recall versus recognition comparison is the strongest test because it relies on the fewest controversial assumptions, and that the other approaches explored by Yonelinas et al. (2002) rely on questionable, theory-laden assumptions. We also rehearse the reasons for concluding that the patients studied by Manns et al. (2003) have damage limited to the hippocampal region (hippocampus proper, dentate gyrus, and subiculum), and we emphasize that important questions remain about the patients studied by Yonelinas et al. (2002), inasmuch as no neuroanatomical information and minimal neuropsychological information has been provided.

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Memory Impairment in Out-of-Hospital Cardiac Arrest Survivors Is Associated With Global Reduction in Brain Volume, Not Focal Hippocampal Injury

Cited by 111 publications

References 28 publications

Recall and recognition are equally impaired in patients with selective hippocampal damage

Recall and recognition are equally impaired in patients with selective hippocampal damage

Lesion evolution in cerebral ischemia

Recall, recognition, and the hippocampus: Reply to Yonelinas et al. (2004)

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