In this review, the clinical, neuropsychological, and neuroimaging findings in the alcoholic Korsakoff syndrome and in thalamic amnesia, resulting from focal infarction, are compared. In both ...disorders, there is controversy over what is the critical site for anterograde amnesia to occur-damage to the anterior thalamus/mammillo-thalamic tract has most commonly been cited, but damage to the medio-dorsal nuclei has also been advocated. Both syndromes show 'core' features of an anterograde amnesic syndrome; but retrograde amnesia is generally much more extensive (going back many years or decades) in the Korsakoff syndrome. Likewise, spontaneous confabulation occurs more commonly in the Korsakoff syndrome, although seen in only a minority of chronic cases. These differences are attributed to the greater prevalence of frontal atrophy and frontal damage in Korsakoff cases.
Alwyn Lishman was interested in how memory research could be applied to clinical psychiatry. After a brief review of his major contributions, this paper will focus on his research on the alcoholic ...Korsakoff syndrome. It will consider how his findings relate to contemporary debates, particularly on how the syndrome should be defined, and its relationship to broader alcohol-induced cognitive impairments.
A review of the contribution of Alwyn Lishman, Robin Jacobson and colleagues to our knowledge of Korsakoff's syndrome, together with a review of the pertinent recent literature.
Lishman and colleagues followed earlier authors in defining the Korsakoff syndrome in terms of disproportionate memory impairment, but they also noted a variable degree of IQ, frontal-executive, and timed visuo-spatial impairment in their cases. More recent authors have included such features in their definitions of the syndrome. Lishman also argued for a specific "alcoholic dementia". The present paper argues that recent definitions of the Korsakoff syndrome confound its core and associated features, and also fail to recognise the multifactorial basis of alcohol-related brain damage.
Korsakoff's syndrome is best defined in terms of disproportionate memory impairment, and more widespread cognitive impairment is best encompassed within "alcohol-related brain damage".
Celotno besedilo
Dostopno za:
BFBNIB, DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, UILJ, UKNU, UL, UM, UPUK
Research on autobiographical memory loss in Alzheimer's disease (AD) is characterized by conflicting findings concerning a possible sparing of older memories. The literature shows evidence for both a ...negative temporal gradient, a flat gradient and a reminiscence bump – that is, a disproportionally high frequency of memories from early adulthood relative to surrounding periods. Here, we expanded the number of lifetime periods of the Autobiographical Memory Interview (AMI; Kopelman, Wilson & Baddeley, 1989, 1990) from the standard three to seven in order to increase the sensitivity of the test to variations in the temporal distribution of autobiographical memories across the life span. Twenty-five older adults diagnosed with AD (MMMSE = 21.16, SD = 5.08) and a matched sample of 30 healthy, older adults were assessed. The temporal distribution for personal semantic information in AD showed a temporal gradient steadily decreasing from middle childhood to present life, consistent with predictions derived from consolidation theories. In comparison, the temporal distribution of incidents/episodic memories produced by AD patients in response to the expanded AMI showed a predominance of autobiographical memories from age 6 to 30, followed by a steep drop in memory referring to events that had occurred after age 30. This distribution challenges standard theories of retrograde amnesia in AD by showing neither a temporal gradient, decreasing progressively from early to later life, nor a flat gradient. In contrast, the distribution is consistent with the reminiscence bump identified in autobiographical memory research. Schematization and retrieval support provided by cultural life scripts are discussed.
Forgetting has been researched for over a century. This literature highlighted how forgetting rates can vary dependent on factors in the design and method. Recent interest in forgetting revived with ...evidence suggesting that seizures experienced almost immediately after matched learning could accelerate forgetting. This was followed by a growth in forgetting studies in patients with temporal lobe epilepsy (TLE), including a subset of those with transient epileptic amnesia (TEA). These patients have been described as expressing concerns about memory, yet often perform within ‘normal’ ranges on standard neuropsychological memory assessments. It was argued that such patients were experiencing a phenomenon termed ‘accelerated long-term forgetting’: apparently normal learning and initial retention with abnormal forgetting over days to weeks after learning. In this review, we critically evaluate aspects of this definition, namely whether learning and initial retention is, in fact, ‘normal’ at first, and further what this means in relation to ‘when’ abnormal forgetting starts. We propose a shift in the understanding of accelerated forgetting in TLE from an emphasis on late-onset forgetting to greater focus on early-onset, progressively greater forgetting. We argue that most evidence from studies to date could be conceptualized within the latter framework, with differences in forgetting patterns reflective of a continuum of severity and/or sensitivity.
This paper begins with a short case report of florid, spontaneous confabulation in a 61-year-old man with an alcohol-induced Wernicke-Korsakoff syndrome. His confabulation extended across episodic ...and personal semantic memory, as well as orientation in time and place, as measured on Dalla Barba's Confabulation Battery. Five other brief case summaries will then be presented, followed by a summary of the clinical, neurological, and background neuropsychological findings in three earlier series of Korsakoff patients. These observations will be considered in light of Wijnia's recent and my own, earlier reviews of the Korsakoff syndrome. Taken together, they indicate the need for a multi-faceted approach (clinical, neurological, neuropsychological, and neuroimaging) to the assessment and diagnosis of the disorder.
Some patients with anosognosia for hemiplegia, i.e. apparent unawareness of hemiplegia, have been clinically observed to show ‘tacit’ or ‘implicit’ awareness of their deficits. Here we have ...experimentally examined whether implicit and explicit responses to the same deficit-related material can dissociate. Fourteen stroke patients with right hemisphere lesions and contralesional paralysis were tested for implicit and explicit responses to brief sentences with deficit-related themes. These responses were elicited using: (i) a verbal inhibition test in which patients had to inhibit completing each sentence with an automatic response (implicit task) and (ii) a rating procedure in which patients rated the self-relevance of the same sentences (explicit task). A group of anosognosic hemiplegic patients was significantly slower than a control group of aware hemiplegic patients in performing the inhibition task with deficit-related sentences than with other emotionally negative themes (relative to neutral themes). This occurred despite their explicit denial of the self-relevance of the former sentences. Individual patient analysis showed that six of the seven anosognosic patients significantly differed from the control group in this dissociation. Using lesion mapping procedures, we found that the lesions of the anosognosic patients differed from those of the ‘aware’ controls mainly by involving the anterior parts of the insula, inferior motor areas, basal ganglia structures, limbic structures and deep white matter. In contrast, the anosognosic patient without implicit awareness had more cortical lesions, mostly in frontal areas, including lateral premotor regions, and also in the parietal and occipital lobes. These results provide strong experimental support for a specific dissociation between implicit and explicit awareness of deficits. More generally, the combination of our behavioural and neural findings suggests that an explicit, affectively personalized sensorimotor awareness requires the re-representation of sensorimotor information in the insular cortex, with possible involvement of limbic areas and basal ganglia circuits. The delusional features of anosognosia for hemiplegia can be explained as a failure of this re-representation.
Disorders of memory KOPELMAN, Michael D
Brain (London, England : 1878),
10/2002, Letnik:
125, Številka:
10
Journal Article
Recenzirano
Odprti dostop
This paper reviews disorders of memory. After a brief survey of the clinical varieties of the amnesic syndrome, transient and persistent, selected theoretical issues will be considered by posing a ...series of questions. (i) What is impaired and what is spared in anterograde amnesia? (ii) Do temporal lobe, diencephalic and frontal lobe amnesias differ? (iii) How independently semantic is semantic memory? (iv) What determines the pattern and extent of retrograde memory loss? (v) Can retrograde amnesia ever be ‘isolated’? (vi) Does psychogenic amnesia involve the same mechanisms as organic amnesia? (vii) How and when do false memories arise? Commonalities as well as differences across separate literatures will be emphasized, and the case for a more ‘dynamic’ (interactionist) approach to the investigation of amnesia will be advocated.
Abstract
Background
The aim was to investigate the co-morbidity profile of people with dementia and examine the associations between severity of co-morbidity, health-related quality of life (HRQoL) ...and quality of life (QoL).
Methods
The improving the experience of Dementia and Enhancing Active Life (IDEAL) cohort consisted of 1,547 people diagnosed with dementia who provided information on the number and type of co-morbid conditions. Participants also provided ratings of their health-related and dementia-specific QoL.
Results
The majority of the sample were living with more than one chronic condition. Hypertension was commonly reported and frequently combined with connective tissue disease, diabetes and depression. The number of co-morbid conditions was associated with low QoL scores, and those with severe co-morbidity (≥5 conditions) showed the greatest impact on their well-being.
Conclusions
Co-morbidity is an important risk factor for poor QoL and health status in people with dementia. Greater recognition of the nature and impact of co-morbidity is needed to inform support and interventions for people with dementia and a multidisciplinary approach to care provision is recommended.
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