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How Inhibition Relates to Impulsivity after Moderate to Severe Traumatic Brain Injury
- Lucien Rochat, Catia Beni, Jean-Marie Annoni, Philippe Vuadens, Martial Van der Linden
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- Journal:
- Journal of the International Neuropsychological Society / Volume 19 / Issue 8 / September 2013
- Published online by Cambridge University Press:
- 02 July 2013, pp. 890-898
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Impulsive behaviors and poor inhibition performances are frequently described in patients with traumatic brain injury (TBI). However, few studies have examined impulsivity and associated inhibition impairments in these patients. Twenty-eight patients with moderate to severe TBI and 27 matched controls performed a stop-signal task designed to assess prepotent response inhibition (the ability to inhibit a dominant or automatic motor response) in a neutral or emotional context and a recent negative task to assess resistance to proactive interference (the ability to resist the intrusion into memory of information that was previously relevant but has since become irrelevant). Informants of each patient completed a short questionnaire designed to assess impulsivity. Patients showed a significant increase in current urgency, lack of premeditation, and lack of perseverance when retrospectively compared with the preinjury condition. Group comparisons revealed poorer prepotent response inhibition and resistance to proactive interference performances in patients with TBI. Finally, correlation analyses revealed a significant positive correlation between urgency (the tendency to act rashly when distressed) and prepotent response inhibition in patients with TBI. This study sheds new light on the construct of impulsivity after a TBI, its related cognitive mechanisms, and its potential role in problematic behaviors described after a TBI. (JINS, 2013, 19, 1–9)
12 - Spasticity and pain after stroke
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- By Philippe Vuadens, Clinique Romande de Réadaptation, Av Grand-Champsec, Michael P. Barnes, Hunters Moor Regional Neurorehabilitation Centre, R. Peyron, Saint-Etienne Center for Pain, Department of Neurology, B. Laurent, Saint-Etienne Center for Pain, Department of Neurology Hôpital de Bellevue,
- 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 286-319
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Summary
Introduction
Since the studies of Sherrington(1947) on decerebrate rigidity in the cat, evidence has shown that spasticity is the result of modification of the sensitivity of the central reflex pathways. Lance defined spasticity in 1980 as a velocity-dependent increase in muscle tone in response to muscle stretch. This resistance to muscle stretch may also result in soft tissue modifications and eventually muscle and soft tissue contractures (Goldspink and Williams, 1990). In this way, it may limit movement and be a significant cause of disability and handicap. Usually spasticity is simply one part of the upper motor neuron syndrome and the other elements of the syndrome are responsible for further disability (Table 12.1).
Spasticity is a dynamic feature that can vary with the position of the limb or trunk, with time, with medication, and with a variety of other factors. Consequently, it is often difficult to evaluate the real impact of spasticity as an independent factor in its own right. The treatment must take into account all the features of the upper motor neuron syndrome, only some of which are responsive to clinical management. The main goal, as always in rehabilitation practice, is to identify the function limited by spasticity and introduce appropriate measures to improve that function. Sometimes a secondary goal can be simply to avoid unnecessary future complications associated with spasticity, such as contractures.
The aim of the first part of this chapter is to discuss the overall context of spasticity in terms of treatment decisions and outcome measures. The general management of spasticity will then be discussed both in terms of physical therapy and orthotic management as well as in terms of oral antispastic medication, focal treatments, and surgery. We will then discuss the management of various types of post-stroke pain, including hemiplegic shoulder pain.
Spasticity
Definition
Lance (1980) defined spasticity as “a motor disorder characterised by a velocity dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting fromhyperexcitability of the stretch reflex, as one component of the upper motor neurone syndrome.” There are three main mechanisms that induce spasticity: modification of the muscle, new nerve collaterals at the spinal level, and exaggeration of the spinal reflexes, which are not appropriatelymodulated by the supraspinal pathways (Brown, 1994; Young, 1994). It is likely that the perturbations of several of these mechanisms are necessary to produce clinical spasticity.
33 - Anterior choroidal artery territory infarcts
- from PART II - VASCULAR TOPOGRAPHIC SYNDROMES
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- By Philippe Vuadens, Julien Bogousslavsky, Department of Neurology, University of Lausanne, Switzerland
- Edited by Julien Bogousslavsky, Université de Lausanne, Switzerland, Louis R. Caplan, Harvard Medical School
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- Book:
- Stroke Syndromes
- Published online:
- 17 May 2010
- Print publication:
- 24 May 2001, pp 451-460
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Summary
Introduction
Since the first reports of an anterior choroidal artery (AChA) infarct by Kolisko in 1891, and Foix et al. in 1925, the clinical pattern of this type of infarction has varied according to isolated cases and small series. The classical triad of Foix et al., consisting of hemiplegia, hemianesthesia, and homonymous hemianopia is rare and it is not specific of the AChA territory (Foix et al., 1925). This clinical pattern can also result from infarction of the deep or superficial branches of the middle cerebral artery (MCA) and the penetrating brainstem arteries. Until the utilization of brain CT scanning in the French studies by Cambier et al. (1983), and Masson et al. (1983), there were less than 25 cases of AChA-territory infarction reported in the literature (Kolisko, 1891; Foix et al., 1925; Cambier et al., 1983; Masson et al., 1983; Poppi, 1928a,b; Ley, 1932; Abbie, 1933a,b; Austregesilo & Borges Fortes, 1983; Steegman & Roberts, 1935; Trelles & Lazorthes, 1939; Hansen & Peters, 1940; Mettler et al., 1954; Morello & Cooper, 1955; Pertuiset et al., 1962; Denecheau, 1963; Fisher, 1965a; Buge et al., 1979; Takahasi et al., 1980; Cooper, 1954). With the development of new radiological technology, infarcts in the AChA-territory have received a new interest (Bruno et al., 1989; Decroix et al., 1986; Ghika et al., 1989; Helgason & Wilbur, 1990; Levy et al., 1995; Leys et al., 1994; Mohr et al., 1991; Paroni Sterbini et al., 1987; Helgason, 1988; Helgason et al., 1986; Hupperts et al., 1994).