Aphasia therapy on a neuroscience basis

Abstract

BACKGROUND: Brain research has documented that the cortical mechanisms for language and action are tightly interwoven and, concurrently, new approaches to language therapy in neurological patients are being developed that implement language training in the context of relevant linguistic and non-linguistic actions, therefore taking advantage of the mutual connections of language and action systems in the brain. A further well-known neuroscience principle is that learning at the neuronal level is driven by correlation; consequently, new approaches to language therapy emphasise massed practice in a short time, thus maximising therapy quantity and frequency and, therefore, correlation at the behavioural and neuronal levels. Learned non-use of unsuccessful actions plays a major role in the chronification of neurological deficits, and behavioural approaches to therapy have therefore employed shaping and other learning techniques to counteract such non-use. AIMS: Advances in theoretical and experimental neuroscience have important implications for clinical practice. We exemplify this in the domain of aphasia rehabilitation. MAIN CONTRIBUTION: Whereas classical wisdom had been that aphasia cannot be significantly improved at a chronic stage, we here review evidence that one type of intensive language-action therapy (ILAT)-constraint-induced aphasia therapy-led to significant improvement of language performance in patients with chronic aphasia. We discuss perspectives for further improving speech-language therapy, including drug treatment that may be particularly fruitful when applied in conjunction with behavioural treatment. In a final section we highlight intensive and rapid therapy studies in chronic aphasia as a unique tool for exploring the cortical reorganisation of language. CONCLUSIONS: We conclude that intensive language action therapy is an efficient tool for improving language functions even at chronic stages of aphasia. Therapy studies using this technique can open new perspectives for research into the plasticity of human language circuits.

Figures

Figure 1.

Neurofunctional links between language and action: Left: Somatotopic sensorimotor activation in pre- and postcentral gyrus during simple repetitive movements of the tongue (in green), index finger (red), and foot (blue). Right: Somatotopic activation during passive reading of action words related to the face (e.g., “lick”, in green), arm or hand (“pick”, red), and leg or foot (“kick”, blue). The somatotopic activation of motor systems reflects aspects of the meaning of the language elements under processing (from Hauk et al., 2004).

Figure 2.

A paradigm for language action therapy: Four partners, usually three patients with aphasia and one therapist, sit around a table and have cards in front of them. Two copies of each card are in the game. There are barriers between the partners, as indicated in the bottom diagram (adapted from Neininger et al., 2004). The participants make requests to obtain a twin card for one they already have, follow requests made by others, reject requests if they cannot follow them, or ask back in case there is a comprehension problem. This interaction follows the normal sequence of these speech acts in dialogues, which is indicated schematically at the top.

Figure 3.

Top: Schematic illustration of long-distance links connecting the cortical areas related to language and action. Motor regions in red, inferior frontal (including Broca's) language area in purple, superior temporal (including Wernicke's) language area in blue. Bottom: A neurobiological model of language–action links: Cell assemblies processing specific language elements, for example action words, may bind information about word forms, which is laid down in perisylvian language cortex, with information about actions, which is laid down in different parts of the motor system (after Pulvermüller, 2005). Abbreviations: A1 = auditory “core” cortex, BPO = Broca, pars opercularis, BPT = Broca, pars triangularis, M1 = motor cortex, PMC = premotor cortex, PFC = posterior prefrontal cortex, WB = Wernicke, auditory belt area, WPB = Wernicke, auditory parabelt area.

Figure 4.

A randomised controlled trial compared one form of intensive language action therapy, Constraint-Induced Aphasia Therapy, to a less intensive conventional treatment. Although the overall number of therapy hours did not differ, the improvement (indicated separately on the right, with standard errors) achieved by patients with chronic aphasia was significantly greater for intensive language action therapy than for the control regime. T-score values calculated from clinical language tests are plotted (Pulvermüller et al., 2001).

Figure 5.

Neurophysiological changes induced by intensive language action therapy in chronic aphasic participants. A brain potential elicited by written words at a latency of ∼250 ms increased significantly over a short therapy period. No comparable change was seen for meaningless pseudowords. The word-specific increase of this “Aphasia Recovery Potential” correlated with the improvement on a clinical language test and its sources were localised in both cortical hemispheres (after Pulvermüller et al., 2005b).