10 / 60
8
ACQ
Volume 12, Number 1 2010
ACQ
uiring knowledge in speech, language and hearing
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
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:
– 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