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Behaviorally spontaneous confabulation in limbic encephalitis: The roles of reality filtering and strategic monitoring
- LOUIS NAHUM, RADEK PTAK, BÉATRICE LEEMANN, PATRICE LALIVE, ARMIN SCHNIDER
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- Journal:
- Journal of the International Neuropsychological Society / Volume 16 / Issue 6 / November 2010
- Published online by Cambridge University Press:
- 19 August 2010, pp. 995-1005
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- Article
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Behaviorally spontaneous confabulation is characterized by a confusion of reality evident in currently inappropriate acts that patients justify with confabulations and in disorientation. Here, we describe a 38-year-old woman lawyer hospitalized because of non-herpetic, presumably autoimmune, limbic encephalitis. For months, she considered herself at work and desperately tried to respect her falsely believed professional obligations. In contrast to a completely erroneous concept of reality, she did not confabulate about her remote personal past. In tasks proposed to test strategic retrieval monitoring, she produced no confabulations. As expected, she failed in tasks of reality filtering, previously shown to have high sensitivity and specificity for behaviorally spontaneous confabulation and disorientation: she failed to suppress the interference of currently irrelevant memories and she had deficient extinction capacity. The observation underscores the special status of behaviorally spontaneous confabulation among confabulatory phenomena and of reality filtering as a thought control mechanism. We suggest that different processes may underlie the generation of false memories and their verbal expression. We also emphasize the need to present theories of confabulation together with experimental tasks that allow one to empirically verify the theories and to explore underlying physiological mechanisms. (JINS, 2010, 16, 995–1005.)
19 - Cognitive recovery after stroke
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- By Antonio Carota, Clinique de Rééducation, University Hospital Geneva, Radek Ptak, Clinique de Rééducation, University Hospital Geneva, Armin Schnider, Clinique de Rééducation, University Hospital Geneva
- Edited by Michael P. Barnes, University of Newcastle upon Tyne, Bruce H. Dobkin, University of California, Los Angeles, Julien Bogousslavsky, Université de Lausanne, Switzerland
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- Book:
- Recovery after Stroke
- Published online:
- 05 August 2016
- Print publication:
- 10 March 2005, pp 503-537
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- Chapter
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Summary
Introduction
Cognitive manifestations of stroke depend primarily on the lesion location. The area of brain destruction partly depends on individual variations in vascular organization, but also on the type of stroke: ischemic stroke tends to produce lesions with relatively stable patterns, defined by the affected vascular territory. Hemorrhages produce damage beyond vascular territories with, nonetheless, preferential lesion distribution: spontaneous intracerebral hemorrhage preferentially occurs in deep structures (basal ganglia, thalamus) or in hemispheric lobes. By contrast, hemorrhage from aneurysm rupture occurs with the arteries at the base of the skull, thus producing specific syndromes, although definitive lesion extension may widely vary with vascular spasms.
The brain's division into vascular territories is only partially congruent with its subdivision in functional neural networks and circuitries. The consequence is that cognitive syndromes caused by ischemic lesions (Table 19.1) are rarely pure and, frequently, several functional systems can be involved (McNeil et al., 1991; Posner, 1995; Robertson, 2001).
It would be beyond the scope of this chapter to discuss in depth the cognitive syndromes occurring after stroke. We will discuss the typical cognitive failures associated with stroke in different cerebral areas as shown in Fig. 19.1 (Schnider, 1997) and then we will focus on some aspects of recovery of the main cognitive disorders occurring after stroke.
Localization of cognitive failures
Prefrontal lesions
Whereas damage of the posterior part of the frontal lobes (motor strip) gives rise to motor syndromes, damage of the area in front of and below the motor strip often produces cognitive and intellectual problems. The prefrontal cortex (Fig. 19.1, area 1) can be defined as the part of the frontal lobes receiving afferents from the dorsomedial thalamic nucleus (Fuster, 1997). It is eminently important for the ability to plan, initiate, and monitor actions; to concentrate on an action; and, at the same time, remain flexible to integrate new incoming information relevant for Behaviors (Fuster, 1997; Miller and Cohen, 2001). The precise cognitive failures emanating from prefrontal damage depend on the lesion location. At least three distinct syndromes can be distinguished (Stuss and Benson, 1986; Cummings, 1993). The first is seen in patients with lesions of the dorsolateral frontal region, following lobar hemorrhage or watershed infarct. They may manifest decreased drive, failure to recognize concepts, and lack of flexibility, together with perseveration and stereotyped motor behavior (e.g. grasping).