Dysarthria is an acquired speech disorder following neurologic injury that reduces intelligibility of speech due to weak, imprecise, slow and/or uncoordinated muscle control. The impact of dysarthria goes beyond communication and affects psychosocial functioning. This is an update of a review previously published by another group in 2005 and has been broadened to include additional interventions.
To assess the effects of interventions to improve dysarthric speech following stroke and other non-progressive adult-acquired brain injury such as trauma, infection, tumour and surgery.
We searched the Cochrane Stroke Group Trials Register (May 2016). We searched CENTRAL (2016, Issue 4 of 12) and we searched the following databases on May 6th 2016: MEDLINE, EMBASE, CINAHL. We searched LLBA (1976 to November 2016) and
PsycINFO (searched 1800 - September 2016). To identify further published, unpublished and ongoing trials, we searched major trials registers WHO ICTRP (http://www.who.int/ictrp/search/en/), the ISRCTN registry (http://www.isrctn.com/), ClinicalTrials.gov (http://www.clinicaltrials.gov/) and the Stroke Trials Registry (www.strokecenter.org/trials/). We also handsearched the reference lists of relevant articles and contacted academic institutions and other researchers regarding other published, unpublished or ongoing trials.
There were no language restrictions.
We selected randomised controlled trials (RCTs) comparing dysarthria interventions with (1) no intervention, (2) another intervention for dysarthria (this intervention may differ in methodology, timing of delivery, duration, frequency or theory), (3) an attention control.
Data collection and analysis
One author (CM) independently screened all titles, three authors (CM, AB, PC) then independently screened remaining abstracts, examined full text studies for possible inclusion and discussed these where necessary, extracted data and assessed risk of bias. We reconciled differences by discussion or through an independent arbitrator. No author reviewed their own study. We contacted study authors for clarification and missing data. We calculated a standardised mean difference (SMD) and 95% confidence interval (CI), using a random-effectsmodel and performed sensitivity analyses to assess the influence ofmethodological quality and planned subgroup analyses for underlying clinical condition.
We retrieved 17,313 citations, identified two ongoing trials and included five small trials that randomised 234 participants. Two studies had low risk of bias and none of the included studies were adequately powered. Two studies used an attention control and three studies compared to an alternative intervention, which in all cases was one intervention versus usual care intervention. There are no trials of an intervention versus no intervention. There are no trials of the same intervention with variations in timing, dose, intensity of treatment. Four studies included only people with stroke, the fifth was predominantly stroke but also brain injury. Three studies delivered intervention in the first few months after stroke, the other two recruited people with chronic dysarthria. Three studies evaluated behavioural interventions, one included acupuncture and one included transcranialmagnetic stimulation.One study included dysarthria as a planned subgroup within a broader trial of impaired communication.
Our primary analysis of a persisting (long lasting i.e. 3-9 months post intervention) effect at the activity level of measurement found no evidence in favour of dysarthria intervention compared to any control (three trials, 116 participants, SMD 0.18, 95% CI -0.18 to 0.55; GRADE: low quality) with zero heterogeneity between trials (I² = 0%). Sensitivity analysis of the studies with low risk of bias found similarly, with a slightly wider confidence interval and slight heterogeneity (two trials, 92 participants, SMD 0.21 (-0.30 to 0.73, I² = 32%; GRADE: low quality). Results of the subgroup analysis for stroke was unsurprisingly similar to the primary analysis as so few non-stroke participants have been recruited to trials (three trials, 106 participants, SMD 0.16, 95% CI -0.23 to 0.54, I² = 0%; GRADE: low quality).
Similar results emerged from most of the secondary analyses. There was no evidence of a persisting effect at the impairment (two trials, 56 participants, SMD 0.07, 95% CI -0.91 to 1.06, I² = 70%; GRADE: very low quality) or participation level (two trials, 79 participants, SMD -0.11, 95% CI -0.56 to 0.33, I² = 0%; GRADE: low quality) but substantial heterogeneity on the former. Analyses of immediate post-intervention outcomes provided no evidence of any short -term benefit on activity (three trials, 117 participants, SMD 0.29, 95% CI -0.07 to 0.66, I² = 0%; GRADE: very low quality); or participation (one study, 32 participants, SMD -0.24, 95%
CI -0.94 to 0.45) levels of measurement.
There was a statistically significant effect favouring intervention at the immediate, impairment level of measurement (four trials, 99 participants, SMD 0.47, 95% CI 0.02 to 0.92, p = 0.04, I² = 0%; GRADE: very low quality) but only one of these four trials had a low risk of bias.
There are no definitive adequately powered randomised controlled trials of interventions for people with dysarthria. There is limited evidence that there may be an immediate beneficial effect on impairment level measures but more, higher quality research is needed to confirm this finding. So although this review evaluated five studies, the benefits and risks of intervention are still unknown and the emerging evidence justifies adequately powered clinical trials into this condition. People with dysarthria after stroke or brain injury should continue to receive rehabilitation according to clinical guidelines.