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29 - Depression after stroke
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- By Antonio Carota, CHUV, Lausanne, Switzerland, Stefano Paolucci, IRCCS Fondazione Santa Lucia, Rome, Italy
- Edited by Olivier Godefroy, Université de Picardie Jules Verne, Amiens, Julien Bogousslavsky, Université de Lausanne, Switzerland
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- Book:
- The Behavioral and Cognitive Neurology of Stroke
- Published online:
- 10 October 2009
- Print publication:
- 18 January 2007, pp 548-570
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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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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).
21 - Depression and fatigue after stroke
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- By Fabienne Staub, Department of Neurology, University of Lausanne, Antonio Carota, 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 556-579
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Summary
Introduction
Post-stroke depression (PSD) is a significant factor affecting functional and social disability, even long after neurological and neuropsychological recovery. Fatigue is a commonly reported complaint in clinical practice. Fatigue after stroke (PSF), often disabling, is frequently reported and can in some cases be the only significant sequelae. It is often neglected or is considered as one aspect of PSD.
Post-stroke depression
The occurrence of PSD has been extensively investigated, with over 200 scientific papers published between 1985 and 1995 (Gordon and Hibbard, 1997). However, major methodological differences between the studies prevent straightforward conclusions being drawn and the following paragraphs are more descriptive than synthetic. For example, PSD has been reported in both less than 25% and in more than 75% of patients. The role of the side and site of stroke also remains controversial.
Diagnosis
The diagnostic accuracy of the standardized psychiatric assessment for patients with neurological impairment is questionable. Psychiatric criteria of mood disorders rely heavily on patients' reports of their own symptoms. This requires patients to be aware of their situation and to be capable of providing an accurate report of it, a task that can be difficult or impossible in patients with aphasia and other cognitive impairment caused by stroke. The presence of neurobehavioral sequelae such as aphasia, psychomotor slowing, anosognosia, and denial often compromises the validity of patients' answers. The presence of conditions interfering with the appreciation of the symptoms of depression should be carefully considered. (Table 21.1).
The diagnosis of mood disorders caused by medical conditions, including stroke, is actually based on the DSM-IV criteria (American Psychiatric Association, 1994). According to these criteria, the diagnosis of PSD requires the presence of persistent symptoms and cannot be made in the very acute phase of stroke. It is also uncertain if the DSM-IV diagnosis of PSD is valid for all depressive episodes occurring at any time after stroke. It is still a subject of controversy whether behavioral changes and subjective symptoms of PSD, and endogenous depression are equivalent (Robertson, 1998) or at least partially different (Lipsey et al., 1986), and whether the two conditions share the dysfunction of the same cerebral areas and neurotransmitters.