The neuropathology of amnesia

Markowitsch, Hans J.; Pritzel, Monika

doi:10.1016/0301-0082(85)90016-4

Cited by 78 publications

(27 citation statements)

References 486 publications

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“…The earliest explanation, suggested by Ribot (1882) and later known as "Ribot's Law" (see Markowitsch & Pritzel, 1985), was that the susceptibility of a particular memory to disruption is inversely proportional to its age. That is, the older a memory is, the more resistant it is to loss due to head injury.…”

Section: Discussionmentioning

confidence: 99%

“…Whereas animal research has repeatedly evaluated consolidationtheory through postlearning experimental manipulationsdesigned to either enhance (drugs) or block (electroshock) the consolidation process (McGaugh, 2000;Riccio & Richardson, 1984), most support for consolidation in humans is derived from the RA that usually accompanies brain trauma resulting from injury, vascular accident (infarct), infection, substance abuse (Korsakoff's), or degenerative neurological disease processes (e.g., Alzheimer's, Parkinson's, Huntington's). Although the phenomenon of RA has been reviewed repeatedly (Hodges, 1995;Kapur, 1993Kapur, , 1999Kopelman, 1989;Levin, Peters, & Hulkonen,1983;Markowitsch & Pritzel, 1985;Sporns & Tononi, 1994), it continues to pose a complex and intriguing mnemonic puzzle for researchers in a number of fields.…”

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confidence: 99%

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Consolidation theory and retrograde amnesia in humans

Brown

2002

Psychonomic Bulletin & Review

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Recent research on the cognitive dysfunctions experienced by human anmesic patients indicates that very long term (multidecade) changes may occur in memory. Flat retrograde amnesia (RA), consisting of a uniform memory deficit for information from all preamnesia time periods, indicates a simple, monolithic retrieval problem, whereas graded RA, with greater memory deficits for information from recent as opposed to remote time periods, suggests the presence of a gradual long-term encoding, or consolidation, process. An evaluation of 247 outcomes from 61 articles provides strong evidence of graded RA across different cerebral injuries, materials, and test procedures, as well as in measures of both absolute and relative (patient vs. control) performance. Future conceptualizationsof human memory should address the possibility that memories increase in resistanceto forgetting, or reduction in trace fragility, across many decades. THEORETICAL AND REVIEW ARTICLES

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Consolidation theory and retrograde amnesia in humans

Brown

2002

Psychonomic Bulletin & Review

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“…The anatomical damage observed in this disorder is predominantly localized to the midline thalamic nuclei, anterior thalamic nuclei, mammillary bodies, and the internal medullary lamina (Aggleton & Pearce, 2001;Langlais & Savage, 1995;Langlais, Zhang, & Savage, 1996;Mair, 1994;Troncoso, Johnston, Hess, Griffin, & Price, 1981). Furthermore, there is evidence of degeneration in key limbic system fiber tracts, such as the mammillothalamic tract and fornix (Langlais & Zhang, 1993;1997), which may lead to potential downstream impairments in other regions of the brain (Jenkins, Dias, Amin, Brown, & Aggleton, 2002;Markowitsch, 1988;Markowitsch & Pritzel, 1985;Reed et al, 2003;Savage, Chang, & Gold, 2003;Vann & Aggleton, 2003;Warrington & Weiskrantz, 1982). The main features of diencephalic amnesia, including those seen in animal models, are severe anterograde learning impairments (Gold & Squire, 2006;Pires, Pereira, Oliveira-Silva, Franco, & Ribeiro, 2005) and long-lasting memory disturbances (Gold & Squire, 2006;Langlais & Savage, 1995;Mair, 1994;Reed et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Impaired, spared, and enhanced ACh efflux across the hippocampus and striatum in diencephalic amnesia is dependent on task demands

Vetreno

Anzalone

Savage

2008

Neurobiology of Learning and Memory

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Diencephalic amnesia manifests itself through a host of neurological and memory impairments. A commonly employed animal model of diencephalic amnesia, pyrithiamine-induced thiamine deficiency (PTD), results in brain lesions and impairments similar in nature and distribution to those observed in humans with Wernicke-Korsakoff syndrome (WKS). In the current investigation, 2 separate experiments were conducted in which acetylcholine (ACh) efflux was assessed in the hippocampus and striatum of PTD-treated and pair-fed (PF) control male Sprague-Dawley rats. The goal was to determine under what behavioral conditions and in which brain structures ACh efflux was spared, impaired, or adaptively enhanced. In Experiment 1, rats were assessed on a spontaneous alternation task; in Experiment 2, rats were tested on a T-maze discrimination task that could be learned via a hippocampal-or striatal-based strategy. In Experiment 1, PTD-treated rats were impaired on the spontaneous alternation task and ACh efflux in the hippocampus during testing was significantly reduced, but spared in the striatum. In Experiment 2, PTD-and PF-treated rats did not differ in the number of trials to criterion, but PTD-treated rats demonstrated greater reliance upon egocentric cues to solve the task. Furthermore, ACh efflux in the striatum was greater during maze learning in the PTD-treated animals when compared to the PF animals. These results suggest that there is behavioral and systems level plasticity that can facilitate the use of alternative strategies to solve a task following diencephalic damage and WKS.

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“…The damage to both key diencephalic nuclei and fiber tracts likely results in a "disconnection syndrome" within the limbic system [see 2,30,59].…”

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Selective septohippocampal – but not forebrain amygdalar – cholinergic dysfunction in diencephalic amnesia

2007

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A rodent model of diencephalic amnesia, pyrithiamine-induced thiamine deficiency (PTD), was used to investigate diencephalic-limbic interactions. In-vivo acetylcholine (ACh) efflux, a marker of memory-related activation, was measured in the hippocampus and the amygdala of PTD-treated and pair-fed (PF) control rats while they were tested on a spontaneous alternation task. During behavioral testing, all animals displayed increases in ACh efflux in both the hippocampus and amygdala. However, during spontaneous alternation testing ACh efflux in the hippocampus and the alternation scores were higher in PF rats relative to PTD-treated rats. In contrast, ACh efflux in the amygdala was not suppressed in PTD treated rats, relative to PF rats, prior to or during behavioral testing. In addition, unbiased stereological estimates of the number of choline acetyltransferase (ChAT) immunopositive neurons in the medial septal/diagonal band (MS/DB) and nucleus basalis of Meynert (NBM) also reveal a selective cholinergic dysfunction: In PTD-treated rats a significant loss of ChAT-immunopositive cells was found only in the MS/DB, but not in the NBM. Significantly, these results demonstrate that thiamine deficiency causes selective cholinergic dysfunction in the septohippocampal pathway. Keywords diencephalon; hippocampus; amygdala; microdialysis; acetylcholine; stereology Selective septohippocampal-but not forebrain amygdalarcholinergic dysfunction in diencephalic amnesiaDiencephalic lesions are seen in a range of disorders: malnourishment, ischemic infarcts, viral infections, tumors and traumatic damage. Damage to certain nuclei and fiber systems within the diencephalon interrupts the flow of information between key memory structures and thus causes severe and long-lasting amnesia [25,29,45]. Although there is evidence that lesions to particular diencephalic nuclei result in memory impairment in their own right, there is also evidence that damage to diencephalic nuclei can disrupt memory circuits leading to dysfunction in other regions of the brain [4,29,45,49,53].Corresponding author: Lisa M. Savage, Department of Psychology, Binghamton University, State University of New York, Binghamton, NY, 13902, e-mail: lsavage@binghamton.edu, fax: 607-777-4890. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. At one point, WKS patients were labeled as "temporal lobe-related amnesiacs" based on their memory performance [10]. This clinical population was critical for the development of the memory system classifications (i.e., declarative vs. nondeclarative memory [51]). However, it is clear from...

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The neuropathology of amnesia

Cited by 78 publications

References 486 publications

Consolidation theory and retrograde amnesia in humans

Consolidation theory and retrograde amnesia in humans

Impaired, spared, and enhanced ACh efflux across the hippocampus and striatum in diencephalic amnesia is dependent on task demands

Selective septohippocampal – but not forebrain amygdalar – cholinergic dysfunction in diencephalic amnesia

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