Recent advances in the treatment of post-stroke aphasia.

Abstract

Aphasia is an impairment of language use following brain damage. There is no consensual definition of aphasia beyond this general description (Code and Petheram, 2011). In a more restricted definition, however, aphasia is an impairment of linguistic processing at the phonological, morphological, lexical semantic or syntactic level which is usually caused by lesions of the left cerebral hemisphere. This impairment can affect language reception and expression depending on the various aphasic syndromes (McNeil and Pratt, 2001). Aphasia results in restrictions in those activities of daily living which rely on communication. In terms of the International Classification of Functioning, Disability and Health (WHO, 2001), limitations in functional communication pose significant challenges to social participation (Davidson et al., 2008) and reduce the patients’ quality of life (Kauhanen et al., 1999; Shadden, 2005). Recent data on the incidence of aphasia following stroke range between 0.02 and 0.06 % with a prevalence between 0.1 and 0.4 % in the developed world (Code and Petheram, 2011). Spontaneous behavioral recovery usually occurs to some degree in the weeks to months after stroke and depends on many factors such as the infarct size and location and the severity of initial stroke deficits (Cramer, 2008). Traditionally, proposed mechanisms of the neurological intrinsic recovery are the resolution of edema surrounding the infarcted area (Katzman et al., 1977; Lo, 1986) and reperfusion of incompletely damaged, but highly vulnerable perilesional tissue (see Donnan et al., 2013). These local mechanisms are supposed to support early recovery (in days to weeks after stroke) and do not depend on behavioral experience but have been targeted by pharmacological treatments: of more than a thousand drugs tested in animal models, 114 have been studied in clinical trials (Perez de la Ossa and Davalos, 2007) and to date none of these potentially neuroprotective agents was found to be effective in humans. Only rapid reperfusion with recombinant tissue plasminogen activator (rTPA) does improve functional outcome after ischemic stroke, but its use is limited by a short therapeutic window (4.5 hours following stroke), the risk of hemorrhage and potential ischemia/reperfusion injury (Lakhan et al., 2009). In contrast, neuronal network reorganization, which also occurs spontaneously, has been related to later recovery and can be influenced by environmental and behavioral factors (Cramer, 2008; Nudo, 2011, 2013). On the molecular level, regulation of gene expression in the unaffected peri-infarct tissue seems to favour the synthesis of growth promoting and to suppress the synthesis of growth inhibiting proteins thus creating a permissive environment for axonal/dendritic sprouting and may thus offer a window of opportunity for behavioural interventions to be effective (Carmichael, 2006). Even after standard treatments provided by the health care systems, the majority of people with aphasia have a chronic communication disability. Speech and language therapy (SLT) is the current standard of care for aphasia treatment but supplemental therapeutic strategies are emerging. The aim of this short review is to give an overview of current advances in research on behavioural, pharmacological and electrophysiological treatments for post-stroke aphasia.