ACQ Vol 12 no 1 2010

speech function. That is, nothing is as beneficial in changing speech, as training in speech itself. The examplars here involved real speech practise (as opposed to isolated oral motor or respiratory function tasks) at each stage of therapy (Murdoch et al., 1999; Morgan et al., 2007). While change may occur due to repetition or practice of salient features, some degree of intensity of practice over a particular duration is thought to be required to effect sustained change. Neither study of interest conducted long- term follow-up assessments to determine the success of carry-over of treatment into the longer-term. Of course data is too scarce to be able to advocate a particular treatment intensity at this stage; however, it is encouraging that treatment programs of 8 sessions over 2 weeks (Murdoch et al., 1999) or 1 session per week for 10 weeks (Morgan et al., 2007) were of sufficient intensity to effect some degree of change at least by the end of the therapy block. Another neural plasticity principle to consider is the onset of treatment . It is likely that the propensity for recovery of dysarthria is greatest during the first 12 weeks post-injury as seen for other disorders such as dysphagia (Morgan, Ward, & Murdoch, 2004) and for general neural recovery (Barnes, 1999) where we typically witness a marked degree of “spontaneous” or rapid recovery. It is typicallly inappropriate to intervene at this stage however due to other medical and cognitive co-morbidities. However, it was heartening that treatment was able to effect positive change in the speech system for as long as up to 5 years post-injury (Murdoch et al., 1999; Morgan et al., 2007). While replication studies are required to confirm the findings of this early work, the preliminary evidence suggests that we should continue to provide patients with systematic, well-designed treatment programs even when referred to us as outpatients with chronic dysarthria. That is, just because the dysarthria is persistent, it may not be intractable. To best illustrate the principle of age effects on training , it would be optimal to compare treatment performance in a group of younger versus older children (e.g., < 5 years vs > 5 years). In fact, some may argue that children in both studies discussed here (aged approximately 10 to 12.5 years at the time of brain injury) actually have adult-like systems and would have consolidated the motor skills for speech prior to the onset of injury. Hence, it could be speculated that these older children have responded to treatment because they found it easier to re-organise or adapt to a previously established skill. Children who sustained injury at earlier ages when they were still developing a particular skill may have found it more challenging to re-acquire or rehabilitate their motor speech function. Again, a lack of evidence precludes us from predicting whether a younger or older age at onset of injury will lead to better or worse outcomes. It is important for future studies in our field to directly consider this issue. The final two neural plasticity principles for consideration are transference and interference of training. The example studies discussed here, being single case studies, are too limited in terms of statistical power to enable us to make a clear decision on whether treating one particular area (e.g., respiration) had a positive or negative impact on other speech sub-systems (e.g., velopharyngeal function). Nevertheless, it is important to keep these principles in mind when designing treatments. For example, one may hypothesise that it would be beneficial to work on the speech sub-systems of respiration and phonation in a single session because the two skills arguably overlap more at a neurophysiological level than other skills, and hence some transference may be expected. It may be hypothesised that working on oral motor and respiratory function together in

Implications for clinical practice The available empirically driven treatment studies in this field are single case (Murdoch et al., 1999) and case series studies (Morgan et al., 2007), and are therefore limited in their generalisability to other patients with ABI. Yet, the preliminary results from both studies are encouraging, with speech improvements being documented post-treatment. Here the two studies are used as a discussion point to illustrate the application of recently outlined principles of neural plasticity (see Kleim & Jones, 2008; Ludlow et al., 2008 for further reference and full definitions of the principles discussed throughout this section) in planning clinical dysarthria intervention for children with ABI. Positive changes in speech function were noted for all four cases across the two studies. None of the cases in these studies had been receiving any form of systematic or regular therapy immediately prior to engagement in the clinical-research study. It is possible at one level therefore that change occurred due to the introduction of a treatment where one had previously been absent. This is elucidatory of the neural plasticity principle of use of function , or “use it or lose it”. What else is special about the application of a specific treatment to enable it to result in change? What other factors should be considered when designing dysarthria treatment? A number of other factors implemented in the two therapy reports discussed here may have helped to effect change, as outlined below. Unlike the random use of speech in daily life, study participants were required to practise or repeat a particular skill using a drill approach, illustrative of the neuroplasticity principle of repetition of training . Children were also required to practise skills that met the principle of being salient or experience specific. For example, some have advocated oral-motor treatment for articulatory-based dysarthric deficits. There has been growing debate however, that oral motor and speech motor function are not controlled by the same neural substrates (e.g., see Ziegler, 2003 for review). As such, it has been suggested that training oral motor function for articulatory impairment in dysarthria (i.e., for sub-types of dysarthria other than flaccid dysarthria where there may well be a weakness of oral motor function) is not experience specific or salient enough to effect changes in – perceptual improvement for phoneme precision and length; spatial EPG measure confirmed improved phoneme precision – intelligibility increased at word and sentence level, with little change reported in everyday speech intelligibility Box 3. Example of treatment summary B (Morgan et al., 2007) • Participants: 3 adolescents (aged 15;0, 14;10 and 15;1 years) with TBI post MVA • Time post-injury: 5, 2.5 and 2.5 years post TBI respectively • Speech diagnoses: mild spastic dysarthria, moderate spastic dysarthria, and severe mixed spastic-ataxic dysarthria (all with severe articulatory deficit) • Study design: case series ABA design • Key therapy goal: increase accuracy of spatial phonetic targets • Treatment technique: a hierarchy of speech tasks (single syllable to sentence level) using electropalatography (EPG) with visual feedback to treat articulatory deficit • Treatment dose: treated for 1 hour, once per week, for 10 weeks • Post-treatment result:

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ACQ Volume 12, Number 1 2010

ACQ uiring knowledge in speech, language and hearing