Biomedical subjects

Peggy Quinette

Publications and source records attributed to Peggy Quinette.

3 recordsLinked to original sources

PubMed2006

The relationship between working memory and episodic memory disorders in transient global amnesia.

In a previous study, we investigated the relationship between the disorders of both episodic memory and working memory in the acute phase of transient global amnesia (TGA). Since executive functions were spared, another dysfunction may be responsible for the binding and maintenance of multimodal informations and contribute to the encoding disorders observed in some patients [Quinette, P., Guillery, B., Desgranges, B., de la Sayette, V., Viader, F., & Eustache, F. (2003). Working memory and executive functions in transient global amnesia. Brain, 126, 1917-1934.]. The aim of this present study was to assess the functions of binding and maintenance of multimodal information during TGA and explore their involvement in episodic memory disorders. We therefore conducted a more thorough investigation of working memory in 16 new patients during the acute phase of TGA using two tasks designed to assess the binding process and both dimensions of the maintenance, namely the active storage and the memory load ability. We also investigated the nature of the episodic memory impairment in distinguishing between the performance of patients with preferential encoding deficits and those of patients with preferential storage disorders on the episodic memory task. This distinction was closely related to the severity of amnesia, i.e. an encoding disorder was observed rather in the early phase of TGA. The results showed that while the functions of binding and maintenance of multimodal information were intact in patients with storage disorders, they were impaired in the case of encoding deficits. These results are interpreted in the recent framework of episodic buffer proposed by Baddeley [Baddeley, A. D. (2000). The episodic buffer: A new component of working memory? Trends in Cognitive Sciences, 4, 417-423] that represents an interface between working memory and episodic memory.

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PubMed2006

What does transient global amnesia really mean? Review of the literature and thorough study of 142 cases.

Since the first reports of transient global amnesia (TGA) were published in 1956, several neuropsychological and functional imaging studies have shed light on different aspects of this neurological syndrome. By establishing diagnostic criteria, Hodges and Warlow (1990b) have made it far easier to identify clinical TGA-related features. However, no comprehensive survey has been yet carried out in order to validate their criteria/findings or provide information about previously unknown features. In the present paper, (i) we review the literature published since Hodges and Warlow's study and seek to characterize the demographic and clinical features of TGA more accurately, (ii) we report 142 personal TGA cases, with supplementary information regarding both episodes and patients, such as precipitating events, associated symptoms and personality, and (iii) we suggest the existence of different groups of TGA patients, on the basis of a hierarchical cluster analysis. This revealed that in women, episodes are mainly associated with an emotional precipitating event, a history of anxiety and a pathological personality. In men, they occur more frequently after a physical precipitating event. In younger patients, a history of headaches may constitute an important risk factor. No link was found with vascular risk factors. The relevance of each of the above-mentioned variables is discussed in the light of our classification. An extensive description of cases from both the literature and our patient population allows us to refine the characterization of clinical TGA features.

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PubMed2003

Working memory and executive functions in transient global amnesia.

Transient global amnesia (TGA) is usually considered to produce a profound impairment of long-term episodic memory, while at the same time sparing working memory. However, this neuropsychological dissociation has rarely been examined in detail. While a few studies have assessed some components of working memory in TGA, the results that have been obtained are far from conclusive. To clarify this issue, we carried out a comprehensive investigation of working memory in 10 patients during a TGA attack. In the first study, we report the results from three patients examined with a battery of neuropsychological tests designed to assess each of the three subcomponents of Baddeley's model of working memory. In a second study, seven different patients underwent neuropsychological investigations that focused specifically on the central executive system, using a protocol derived from a study by Miyake and colleagues. Our findings showed that subcomponents of working memory, such as the phonological loop and visuo-spatial sketch pad, were spared in TGA patients. Specific executive functions that entailed inhibitory control, dual task performance, updating and shifting mechanisms were also found to be normal. However, we found significantly impaired performance for the Brown-Peterson test, and that TGA patients were significantly impaired in the recollection of their episodic memories. They also made reduced numbers of 'remember' compared with 'know' judgments in the episodic memory test several days after TGA. On the basis of our findings, it would appear that the episodic memory deficit during TGA is not related to elementary aspects of executive functioning. Our data also highlight the nature of the cognitive mechanisms involved in the Brown-Peterson task, which may well depend on long-term memory (such as the process of semantic encoding). Lastly, the selective deficit in recollective episodic memories observed in TGA may be principally related to medial temporal lobe abnormalities that have been reported in this syndrome.

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