One such debate centers on the dissociation of neurocognitive processes underlying fundamental aspects of anterograde retrieval. We propose that network abnormalities are key to understanding inconsistencies that underpin central debates about HPC function in amnesia research. These abnormalities may be important in understanding memory impairment in neurological disease ( Addis et al., 2007) but their explanatory potential is under-explored.
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Indeed, broader network abnormalities are well documented in other ‘focal’ conditions and have been demonstrated in small case series of amnesic patients ( Hayes et al., 2012 Henson et al., 2016 Rudebeck et al., 2013). Such studies have been criticized for attributing behavioral deficits solely to the HPC ( Squire and Wixted, 2011), despite the fact that focal damage may trigger more subtle structural and functional abnormalities across an extended HPC system, involving the thalamus and cingulate cortex ( Aggleton, 2014).
Studies of amnesic patients have, however, often produced inconsistent results. ( Scoville and Milner, 1957), hippocampal (HPC) amnesia has played a fundamental role in the neuroscience of human memory ( MacPherson and Della Sala, 2019). IntroductionĮver since the first report of the famous patient H.M. Network abnormalities may explain the variability across studies of amnesia and speak to debates in memory neuroscience. Associations of hippocampal volume with recall, recognition, and remote memory were fully mediated by wider network abnormalities, and were only direct in forgetting. Besides hippocampal atrophy, we observed correlatively reduced thalamic and entorhinal cortical volume, resting-state inter-hippocampal connectivity and activity in posteromedial cortex. These patients showed impaired recall, recognition and maintenance of new information, and remote autobiographical amnesia.
We assessed this hypothesis in a uniquely large cohort of patients (n = 38) after autoimmune limbic encephalitis, a syndrome associated with focal structural hippocampal pathology. We hypothesized that focal hippocampal damage is associated with changes across the extended hippocampal system and that these, rather than hippocampal atrophy per se, would explain variability in memory between patients. Patients with hippocampal amnesia play a central role in memory neuroscience but the neural underpinnings of amnesia are hotly debated.
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