Articles

Behavioural intervention for dysphagia in acute stroke:

a randomised controlled trial
Giselle Carnaby, Graeme J Hankey, Julia Pizzi

Summary
Background Swallowing dysfunction after stroke is common, but there is little reliable evidence for how the disorder
should be managed. This study compared standard low-intensity and high-intensity behavioural interventions with
usual care for dysphagia.
Methods 306 patients with clinical dysphagia admitted to hospital with acute stroke were randomly assigned to
receive usual care (n=102), prescribed by the attending physician; standard low-intensity intervention (n=102),
comprising swallowing compensation strategies and diet prescription three times weekly for up to a month; or
standard high-intensity intervention and dietary prescription (n=102), at least daily for up to a month. The primary
outcome measure was survival free of an abnormal diet at 6 months. Analysis was done by intention to treat. This
study is registered with ClinicalTrials.gov, number NCT00257764.
Findings 60 patients died and three patients were lost to follow up before the 6-month analysis. Of patients randomly
allocated usual care, 56% (57/102) survived at 6 months free of an abnormal diet compared with 67% (136/204)
allocated standard swallowing therapy (relative risk 119, 95% CI 098145). Standard swallowing therapy was
associated with a non-signicant trend toward a reduction in death (080, 0513), institutionalisation (069,
0411), and dependency (105, 0813); a signicant reduction in swallowing-related medical complications
(073, 0609), chest infection (056, 0408), and death or institutionalisation (073, 055097); and a
signicant rise in the proportion of patients regaining swallowing function (141, 103194) by 6 months.
Compared with usual care and low-intensity therapy, high-intensity therapy was associated with an increased
proportion of patients who returned to a normal diet (p=004) and recovered swallowing (p=002) by 6 months.

Lancet Neurol 2006; 5: 3137

Published online
November 30, 2005
DOI:10.1016/S1474-4422(05)
70252-0
Department of Psychiatry,
University of Florida, Florida,
USA (G Carnaby PhD);
Stroke Unit, Department of
Neurology, Royal Perth
Hospital, WA, Australia
(G Hankey FRACP, J Pizzi BSc);
and School of Medicine and
Pharmacology, University of
Western Australia, WA,
Australia (G Hankey FRACP)
Correspondence to:
Giselle Carnaby (ne Mann)
gmann@pyschiatry.u.edu

Interpretation These data show a consistent trend towards more favourable outcomes in dysphagic stroke patients
who are assigned a standard programme of early behavioural swallowing intervention, including active therapeutic
approaches and dietary modication.

Introduction
Swallowing disorders (dysphagia with or without
aspiration) are present in about 2750% of patients with
acute stroke,15 and are associated with an increased risk
of complications, such as aspiration pneumonia,
dehydration, and malnutrition, in a fth to a third
of patients.1,6,7 These complications are theoretically
preventable by prompt and accurate diagnosis of the
swallowing disorder and appropriate intervention. The
possible interventions include indirect behavioural
strategies (eg, modication of food consistency),8 direct
behavioural strategies (eg, stimulation of oral and
pharyngeal structures),9 and enteral feeding by means of
a nasogastric tube or by percutaneous endoscopic
gastrostomy.1013
Feeding by percutaneous endoscopic gastrostomy is
associated with an increased rate of death or a poor
outcome compared with feeding by nasogastric tube.11,12
The effectiveness of behavioural interventions for
swallowing disorders after stroke, however, is uncertain.
Kasprisin and colleagues14 did a non-randomised,
uncontrolled study of swallowing therapy in patients
with stroke and mixed neurogenic causes (n=69). The
main outcome of this study was pneumonia
development as reported from chart review. Despite the
http://neurology.thelancet.com Vol 5 January 2006

inclusion of unmatched comparison groups with mixed

causes, the authors concluded that swallowing therapy
was efcacious. Rosenbek and co-workers15 undertook a
controlled, multiple crossover design assessment of the
effect of thermal stimulation of the fauces on
swallowing in seven patients with multiple previous
strokes. They identied initial change in duration and
descriptive measures of swallowing; however, these
changes were not maintained a month after treatment.
From a different focus, Sukthankar and colleagues16 did
a randomised controlled trial of nine patients with
dysphagia secondary to stroke or head injury. Patients
were randomised to receive treatment with oral
exercises or oral exercises with visual and audio
biofeedback. These authors concluded that oral exercises
combined with biofeedback methods improved
swallowing recovery, despite including only lip and
tongue force measures as outcomes. DePippo and
co-workers17 studied 115 orally fed patients with subacute stroke, mild dysphagia, and absent or minimum
aspiration on videouoroscopy. Patients were randomly
assigned to one of three graded levels of treatment,
including dietary modication and swallowing therapy.
However, the study did not include a non-treatment
control group. Outcome measures included pneumonia,
31

Articles

dehydration, calorie-nitrogen decit, and death. The

authors concluded that outcome did not differ among
the three groups. Furthermore, only 15% of patients
reached one or more of these endpoints within the
12-month study period.
Taken together these studies suggest positive
outcomes from behavioural interventions for dysphagia.
However, signicant design issues make it impossible
to conclude efcacy for this form of intervention;
specically, small sample sizes,1417 restriction to patients
with a narrow spectrum17 or multiple causes of
dysphagia,14,16 and limitation by delayed intervention15 or
lack of a control group.15,17
The primary aim of this study was to ascertain whether
a standard behavioural intervention for swallowing
dysfunction after stroke, given by a speech pathologist
for up to a month after stroke, could improve swallowing
function, as measured by the proportion of patients
returning to a normal (prestroke) diet by 6 months after
stroke, compared with usual care in hospital. Secondary
aims were to determine a) whether the intervention
could increase the proportion of patients who recovered
swallowing function and reduce the proportion who
developed dysphagic-related complications, died, were
institutionalised, or dependent in activities of daily living
by 6 months after stroke; and b) whether there was
a dose-dependent effect associated with high-intensity
and low-intensity standard behavioural interventions.

Methods
Patients
The study was undertaken in a university teaching
hospital, the Royal Perth Hospital, which provides
medical services for the eastern suburban region of
Perth, Western Australia. All patients presenting to the
Royal Perth Hospital over a 3-year period were screened
for inclusion in the study. Patients were included if a
clinical diagnosis of stroke was conrmed by the
attending clinician (GJH), according to the WHO
denition of stroke;18 if the onset of stroke was within the
previous 7 days; if the study speech pathologist (JP)
made a clinical diagnosis of swallowing difculty
(dysphagia), as measured by a score of less than 85 on
the Paramatta Hospitals assessment of dysphagia;1921 if
the patient had no history of swallowing treatment or
surgery of the head or neck; and if the patient gave
written informed consent to participate in the trial and
be followed up for the next 6 months. Patients for whom
consent could not be gathered were placed on a waiting
list, reassessed daily, and included if they met the entry
criteria and consented within 7 days of stroke onset.
Eligible patients underwent a baseline assessment of
demography, comorbidity, premorbid function, clinical
stroke syndrome, stroke pathology, stroke subtype, and
results of CT and MRI brain scans. Stroke severity was
measured according to the modied Rankin score22 and
the modied Barthel index,23 and swallowing function
32

(PHAD score) and the type and method of oral intake

were also reported. An instrumental assessment of
swallowing function, by means of videouoroscopy, was
done routinely in patients assigned to the high-intensity
and low-intensity treatment groups; patients allocated
usual care were managed at the discretion of the
attending clinician.
The study protocol was approved by the ethics
committee and institutional review board of Royal Perth
Hospital.

Procedures
Randomisation was undertaken by use of a block
randomisation technique. The treatment allocation was
based on a computer-generated random numbers list
generated with the SPSS statistical package (version
9.0). The randomisation schedule was held in the trial
ofce, remote from the study environment. After clinical
assessment by the study speech pathologist (JP), eligible
patients were informed about the trial and, after
providing informed consent, were randomly assigned to
one of three treatment options by means of a telephone
call to the trial ofce by the study speech pathologist.
The three treatment groups were usual care, standard
low-intensity treatment, and standard high-intensity
treatment. Usual care (control) consisted of patient
management by the attending physicians as per usual
practice. Physicians referred their patients to the
existing hospital speech pathology service if they
considered it to be appropriate. Treatment, if offered,
consisted mainly of supervision for feeding and
precautions for safe swallowing (eg, positioning, slowed
rate of feeding). Videouoroscopic assessment of
swallowing function was undertaken only if prescribed
by the attending physician.
Standard low-intensity swallowing therapy was
composed of swallowing compensation strategies,
mainly environmental modications (eg, upright
positioning for feeding); safe swallowing advice (eg,
reduced rate of eating); and appropriate dietary
modication, under the direction of the study speech
pathologist, three times per week for a month, or for the
duration of the hospital stay (if less than a month). The
choice of specic swallowing compensation strategies
was directed by the ndings of the clinical swallowing
examination and videouoroscopy (at baseline and at
follow up, if necessary).
Standard high-intensity swallowing therapy consisted
of direct swallowing exercises (eg, effortful swallowing,
supraglottic swallow technique) and appropriate dietary
modication, under the direction of the study speech
pathologist, every working day for a month or daily for
the duration of the hospital stay (if less than a month).
The choice of specic swallowing exercises was
established by the ndings of the clinical examination
and videouoroscopy (at baseline and at follow up, if
necessary).
http://neurology.thelancet.com Vol 5 January 2006

Articles

All people involved in the study were unaware of the

treatment allocation, apart from the patients and the
study speech pathologist who treated the patients
assigned to the high-intensity and low-intensity groups.
The study speech pathologist, who assessed all stroke
admissions for eligibility in the trial, worked
independently of the hospital speech pathology service
and did not share any trial information with the hospital
therapists. The hospital speech pathology service
continued to receive sporadic referrals from the hospital
physicians, as per usual practice, and some of these
patients had been enrolled in the trial and assigned usual
care. The physicians were not informed if their patients
had been randomly assigned to usual care in the trial.
Clinical neurological assessments and grading of CT
and MRI brains scans were done by the study neurologist
(GJH) before randomisation. All patients were cared for
in the stroke unit, the general neurology ward, or the
general medical wards.
Outcome was assessed by an independent speech
pathologist (GC), who was unaware of the treatment
allocation, every month for 6 months after randomisation.
Inpatient progress and the occurrence of any possible
complications were sought from multiple overlapping
sources, such as asking patients, relatives, and staff at
each monthly assessment. Information about treatment
was not requested and treatment records were not
reviewed to maintain masking. Outcome after hospital
discharge was recorded by the patient or caregiver in a
dedicated diary, and veried, if necessary, by the patients
community doctor and reviewed at each monthly contact.
The primary outcome measure was the proportion of
patients who returned to their normal prestroke diet
within 6 months after randomisation. Secondary outcome
measures included the time to return to a normal diet; the
proportion of patients who had recovered functional
swallowing or developed one or more dysphagia-related
medical complications (such as chest infection,
dehydration, calorie-nitrogen decit); and the proportion
of patients who had died, were institutionalised, or
dependent in activities of daily living by 6 months after
stroke.
Abnormal diet was dened as dietary intake (oral or
non-oral) needing a restricted consistency or special
preparation before it could be consumed safely.
Functional swallowing was dened as a return to
prestroke diet without swallowing complications. Chest
infection was dened as at least three of: fever more
than 38C; productive cough; abnormal respiratory
examination (tachypnoea 22 breaths per min,
tachycardia, inspiratory crackles, bronchial breathing);
arterial hypoxaemia (PaO293kPa); culture of a relevant
pathogen; and positive chest radiograph in a patient with
suspected chest infection. Dehydration was dened as
loss of total bodyweight (10%), postural hypotension
(30 mm Hg), urea to creatinine ratio greater than
123 mmol/L, or serum sodium more than 145 mmol/L
http://neurology.thelancet.com Vol 5 January 2006

3227 suspected clinical strokes

2356 ineligible
460 not notified of study
92 discharged/outside window
595 not dysphagic
1041 non-stroke diagnosis
90 died before assessment
78 inappropriate

871 eligible

565 not randomised

136 refused consent
61 died before randomised
71 discharged before randomised
53 not notified
244 enrolled in other trials

306 randomised

102 assigned high-intensity

treatment (1 non-stroke)

102 assigned low-intensity

treatment (2 non-stroke)

102 assigned usual care

(1 non-stroke)

17 died at 6 months
2 lost to follow up

20 died at 6 months
1 lost to follow up

23 died at 6 months

Analysed for endpoints:

94 at 1 month
81 at 6 months

Analysed for endpoints:

92 at 1 month
79 at 6 months

Analysed for endpoints:

94 at 1 month
83 at 6 months

Figure 1: Trial prole

Demographics
Age, years
Sex, male
Clinical syndrome
Total anterior circulation syndrome
Partial anterior circulation syndrome
Lacunar syndrome
Posterior circulation syndrome
Unknown/non-stroke
Pathology
Cerebral infarction
Cerebral haemorrhage
Unknown
Stroke severity
Barthel index 15
Barthel index 15
Stroke handicap
Rankin score 3
Rankin score 3
Length of hospital stay, days

High intensity
(n=102)

Low intensity
(n=102)

Usual care
(n=102)

698 (125)
60 (59%)

72 (124)
59 (58%)

714 (127)
59 (58%)

36 (35%)
34 (33%)
23 (23%)
8 (8%)
1 (1%)

30 (29%)
35 (34%)
25 (25%)
10 (10%)
2 (2%)

42 (41%)
30 (29%)
19 (19%)
10 (10%)
1 (1%)

93 (91%)
8 (8%)
1 (1%)

90 (88%)
10 (10%)
2 (2%)

90 (88%)
11 (11%)
1 (1%)

80 (78%)
22 (22%)

80 (78%)
22 (22%)

81 (79%)
21 (21%)

15 (15%)
87 (85%)
191 (105)

21 (21%)
81 (79%)
192 (133)

17 (17%)
85 (83%)
214 (124)

Data are number (%) or mean (SD).

Table 1: Baseline characteristics

33

Articles

Videouoroscopic swallowing assessment

Swallowing treatment sessions
Duration of treatment per session, min
Days treatment provided*

High intensity Low intensity

Usual care

ANOVA

81 (79%)
116 (63)
242 (76)
114 (65)

28 (27%)
48 (39)
160 (92)
179 (87)

51
389
20

00001
00001
0001

88 (86%)
78 (38)
248 (67)
167 (79)

Data are number (%) or mean (SD). *Data are for patients who received treatment and do not include those who received none.

Table 2: Swallowing intervention, by treatment group

Primary outcome at 6 months

Normal diet
Secondary outcomes at 6 months
Functional swallowing
Any complication
Chest infection
Death
Institutionalisation
Dependency (Rankin3)
Death or institutionalisation
Death or dependency

Usual care
(n=102)

Standard swallowing
therapy (n=204)

Relative risk (95% CI)

57

136

119 (098145)

33
64
48
23
26
49
49
72

93
94
54
37
36
103
72
140

141 (103194)
073 (060092)
056 (041076)
080 (04913)
069 (04311)
105 (08213)
073 (055097)
097 (08311)

Data are number of patients.

Table 3: Comparison of organised swallowing therapy (high-intensity and low-intensity groups

combined) versus usual care

not due to renal insufciency or use of diuretics. Calorienitrogen decit was dened as serum albumin less
than 25 g/L or sustained ketonuria without glycosuria.
Dependency was dened as a modied Rankin scale score
of 3 or more or a Barthel index score of 15/20 or less.

improve this rate by 20% in absolute terms to 90% at

6 months. In order to have 80% power at the 5% (two
tailed) signicance level to reliably identify this treatment
effect or larger, the sample size needed was estimated to
be 300 (100 in each group).
Analyses were by intention to treat. Therefore, all
306 patients who were randomised were included in the
analysis, including the four patients who were subsequently deemed to have not had a stroke.
Parametric statistical tests (eg, t tests) were undertaken
for normally distributed variables, and non-parametric
tests (eg, Mann Whitney U tests) were done for skewed
variables. Odds ratios and their 95% CIs were derived for
all primary and secondary outcomes. Logistic regression
models were tted to each of the main binary endpoints.
Rank data and other continuous endpoints were reviewed
by ANOVA. The 2 test was used for discrete counts of
patients with particular categories of adverse and dietary
events. In our protocol the primary comparison of interest
was that between the standard treatment and usual care
groups; a trend analysis was also done using 2 for linear
trend in proportion for all three groups. Differences in the
Kaplan-Meier curves were analysed with log rank tests.
This study is registered with ClinicalTrials.gov, number
NCT00257764.

Role of the funding source

The sponsor of the study had no role in study design,
data collection, data analysis, data interpretation, or
writing of the report. The corresponding author had full
access to all the data in the study and had nal
responsibility for the decision to submit for publication.

Statistical analysis
The study sample size calculations were based on our
earlier nding that 87% of patients with dysphagia after
rst-ever acute stroke returned to a normal diet by
6 months.7 Because many of these patients with mild
stroke had been treated with standard behavioural
swallowing therapies, we postulated that about 70% of
patients assigned usual care in this study would have a
6-month survival period free of an abnormal diet and that
assignment to standard swallowing therapy would

Primary outcome at 6 months

Normal diet
Secondary outcomes at 6 months
Functional swallowing
Chest infection
Any complication
Death
Institutionalisation
Dependency (Rankin3)
Death or institutionalisation
Death or dependency

Usual care

Low intensity

High intensity

57

65

71

004

33
48
64
23
26
72
49
72

44
26
44
20
17
68
36
69

49
28
50
17
19
69
36
72

002
0003
005
029
022
065
006
087

Data are number of patients.

Table 4: Comparison of high-intensity versus low-intensity speech therapy versus usual care

34

Results
A total of 3227 patients with suspected strokes were
referred to the study team between May 1, 1996, and
May 31, 1999, of whom 27% were eligible for inclusion
in the study (gure 1). Written informed consent was
obtained from 306 (35%) of the 871 eligible patients.
Ineligible patients did not differ signicantly from
enrolled patients in severity of stroke or dysphagia.
Table 1 shows the baseline characteristics of the patients.
The mean time to admission was 8 h after stroke onset
and to randomisation was 27 days after stroke onset for
all treatment groups. The mean duration of hospital stay
did not differ between the three groups.
The number of swallowing therapy sessions and the
duration of sessions for patients assigned to the
standard treatment groups were signicantly greater
than for those assigned to the usual care group (table 2).
The number of days over which patients received
swallowing therapy was signicantly less in the standard
treatment groups than in the usual care group.
Follow up at 6 months was complete for 243 (99%) of
the 246 survivors. Data for the 60 patients who died and
three patients lost to follow up at 56 days, 110 days,
and 163 days after randomisation, respectively, were
http://neurology.thelancet.com Vol 5 January 2006

Articles

censored for time spent in the study and included in the

intention-to-treat analysis (gure 1).
Of the 102 patients randomly allocated usual care, 56%
survived free of an abnormal diet at 6 months after
stroke compared with 67% of the 204 patients allocated
standard swallowing treatment (table 3). Of patients
allocated high-intensity swallowing treatment, 70%
survived free of an abnormal diet at 6 months after
stroke, compared with 64% of patients allocated lowintensity swallowing treatment and 56% of patients
assigned usual care (table 4). The time to return to a
normal diet was signicantly shorter for patients
assigned usual care compared with standard swallowing
treatment (F=34, p003). Kaplan-Meier survival
curves for the three groups, however, were not
signicantly different (gure 2).
Of patients allocated standard swallowing therapy,
46% achieved prestroke swallowing function at
6 months compared with 32% of patients allocated usual
care (table 3). Among patients allocated the highintensity swallowing intervention, 48% achieved
prestroke swallowing function at 6 months compared
with 43% of patients allocated the low-intensity
swallowing intervention and 32% of patients assigned
usual care (table 4).
Among patients allocated standard swallowing
therapy, 46% experienced a swallowing-related medical
complication within the rst 6 months after stroke
compared with 63% of patients allocated usual care
(table 3). Most complications avoided by swallowing
therapy were chest infection due to aspiration (47%
usual care vs 26% organised care). Signicantly fewer
patients allocated standard swallowing therapy (36%)
than usual care (48%) were dead or institutionalised at
6 months.

10

Cumulative survival

08

06
High intensity
Low intensity
Usual care

04

02
Log rank test p=046
00
0

50

100

150

Days follow up after randomisation

Numbers at risk
High intensity 102
Low intensity 102
Usual care
102

42
44
40

23
32
19

Figure 2: Time to survival free of an abnormal diet

http://neurology.thelancet.com Vol 5 January 2006

14
22
8

Discussion
The results of this study do not lend support to the
primary study hypothesis that a standard programme of
swallowing therapy given early to patients with acute
stroke and maintained as required, is associated with a
signicant increase in the proportion of patients who
survive free of an abnormal diet by 6 months after
stroke. Furthermore, there was no signicant effect of
swallowing therapy on death, institutionalisation, and
dependency at 6 months after stroke. However, the study
did show a consistent, albeit non-signicant, trend in
favour of swallowing therapy versus usual care for these
outcomes, and a signicant rise in the proportion of
patients who achieved functional swallowing and a
decrease in the proportion of patients who had a
dysphagia-related medical complication (especially
aspiration pneumonia) and died or needed
institutionalisation (as a combined outcome) by
6 months after stroke. A doseresponse relation was also
apparent with a signicant trend toward improved
recovery of swallowing function and less chest infection
in patients randomly allocated intensive standard
swallowing therapy than in those allocated less intensive
therapy and usual care.
The strengths of this study are the reduced systematic
bias in treatment allocation by randomisation, reduced
observer bias in outcome assessment by the masking of
the outcome assessor to the treatment allocation, and the
minimisation of random error by the relatively large
number of patients and outcomes studied.
There are several weaknesses of this study. The rst is
that the patient and the treating therapist were aware of
the treatment allocation, which introduces the
possibility of bias in the way treatment was delivered to
certain patients and the way patients reported subjective
outcomes. The most likely systematic error was that
patients assigned usual care could have been treated
with a more standard approach by hospital therapists
because they may have indirectly learnt about the
ongoing trial and observed how other enrolled patients
were being treated, thus biasing the results toward the
null hypothesis. We believe that the patients awareness
of treatment allocation was unlikely to have biased the
results because 59% of patients discharged from
hospital were unable to identify the nature of the
swallowing treatment they received. Furthermore,
patient outcome recording bias is unlikely to have
affected rates of objective outcomes, such as medical
complications (eg, chest infection), death, and
institutionalisation. Finally, the independent outcome
assessor, who recorded patient diet progress and
swallowing function, was able to predict the treatment
allocation correctly in only 29% of patients (Kappa 032).
Another potential weakness is that, despite this being
the largest randomised trial of any behavioural
swallowing intervention in acute stroke, the numbers of
patients and outcome events were still rather small. As a
35

Articles

result, our estimates are imprecise with wide 95% CIs,

introducing the possibility that our results could be due
to chance. However, the qualitative consistency of the
results across several outcome events (ie, all favouring
standard treatment) is suggestive of a true positive
treatment effect, but the size of the treatment effect
remains imprecise.
A nal limitation of our study is that it was undertaken
in a single centre with hospital-referred patients with
moderate to severe stroke. The generalisability (external
validity) of the results to other therapists and patients
therefore remains uncertain. However, our intervention
is clearly described and our patients are typical of
those who have swallowing dysfunction after stroke.
Additionally, our study yielded a mean age of patients
with stroke (71 years) that is younger than the currently
reported mean age for stroke in the USA (77 years). We
believe, however, that our mean age and range are
representative of the Australian population. Australia is
a large country with many diverse population groups.
The age and sex distribution, together with ethnic
mix and lifestyle factors, affects our ndings. In our
study, 5% of the study sample was from pan-Asian
background. Recent Asian stroke studies have also
identied a lower mean age for stroke.24 Moreover, a
review of the mean stroke age from studies that used
analogous Australian samples shows comparable
results.2527
The faster time to return to a normal diet among
patients allocated usual care could be due to the fact that
52 of the 102 patients assigned usual care were
immediately prescribed a normal diet on admission by
ward staff, without waiting for an assessment of
swallowing function by a speech and swallowing
therapist. This was a common observation in our
previous studies5,7 and was one of the reasons for our
study hypothesis that usual care would be associated
with a failure to diagnose unobvious swallowing
dysfunction in some patients and predispose such
patients to a high risk of aspiration pneumonia.
Differences in time to achieve certain diet levels might
also be strongly affected by care practices (eg,
perceptions of the staff or involvement of a swallowing
clinician, rather than the patients functional feeding
ability alone).
Our trial was not powered to reliably identify or
exclude a doseresponse relation between intensity of
swallowing therapy and outcome. Because the results of
the low-intensity and high-intensity groups were not
strikingly different from one another, it is not possible to
determine whether there is a differential treatment
effect and whether low-intensity treatment could be as
effective as high-intensity treatment.
The only other truly randomised trial of behavioural
swallowing therapy after stroke reported no signicant
effect of graded levels of instruction regarding types of
food and the manner of intake on swallowing-related
36

outcomes in 115 dysphagic stroke patients admitted to a

subacute rehabilitation centre.17 However, this study did
not include a control group, patients were assessed a
mean of 45 weeks after their stroke, and the number of
outcome events was very small.17
The results of our study provide reasonably reliable
data, which lend support to the potential value of
behavioural swallowing intervention after acute stroke to
help with the return to prestroke swallowing function
and minimisation of dysphagia-related adverse
outcomes. These encouraging results might be
attributed to the quality and quantity of the intervention;
patients assigned to the standardised swallowing care
groups were treated more frequently and for longer
durations (ie, more intensively) over a shorter period of
time than were those assigned usual care. If these
results can be replicated in other settings, they would
suggest that the management of patients with acute
stroke should include a dedicated, standard programme
of early behavioural swallowing intervention, composed
of active therapeutic approaches as well as dietary
modication.
Acknowledgments
This study was supported by an educational grant from the Royal Perth
Hospital Medical Research Foundation.
Authors contributions
GC participated in the development and design of the study, conducted
and supervised assessments and procedures within the study, reviewed
and interpreted data, and participated in the development of the
manuscript. GJH participated in the design of the study, conducted and
supervised neurological assessments and procedures, reviewed and
interpreted data, and participated in the development of the manuscript.
JP participated in the management of the study, conducted speechlanguage pathology treatments and procedures, reviewed and interpreted
data included in the study, and participated in development of the
manuscript.
Conicts of interest
We have no conicts of interest.
References
1
Gordon C, Hewer RL, Wade DT. Dysphagia in acute stroke. BMJ
1987; 295: 41114.
2
Wolfe C, Taub N, Woodrow J, Richardson E, Warburton F,
Burney P. Patterns of acute stroke care in three districts in
southern England. J Epidemiol Commun Health 1993; 47: 14448.
3
Odderson IR, Keaton JC, McKenna BS. Swallow management in
patients on an acute stroke pathway: quality is cost effective.
Arch Phys Med Rehab 1995; 76: 113033.
4
Smithard D, ONeill P, Park C, et al. Complications and outcome
after acute stroke: does dysphagia matter? Stroke 1996: 27: 120004.
5
Mann G, Hankey GJ, Cameron D. Swallowing disorders after acute
stroke: prevalence and diagnostic accuracy. Cerebrovasc Dis 2000;
10: 38086.
6
Smithard DG, ONeill PA, England RE, et al. The natural history of
dysphagia following a stroke. Dysphagia 1997; 12: 18893.
7
Mann G, Hankey GJ, Cameron D. Swallowing dysfunction after
acute stroke: prognosis and prognostic factors at 6 months. Stroke
1999; 30: 74448.
8
Logemann J. Approaches to management of disordered
swallowing. Clin Gastroenterol 1991; 5: 26980.
9
Lazarra G, Lazarus C, Logemann J. Impact of thermal stimulation
on the triggering on the swallow reex. Dysphagia 1986; 1: 7377.
10 Finestone HM. Safe feeding methods in stroke patients. Lancet
2000; 355: 166263.
11 FOOD Trial Collaboration. Effect of timing and method of enteral

http://neurology.thelancet.com Vol 5 January 2006

Articles

12
13

14
15

16

17

18

tube feeding for dysphagic stroke patients (FOOD): a multicentre

randomised controlled trial. Lancet 2005; 365: 76472.
Bath PMW, Bath FJ, Smithard DG. Interventions for dysphagia in
acute stroke. Cochrane Database Syst Rev 2004; 4: CD 000323.
Norton B, Homer-Ward M, Donnelly MT, Long RG, Homes GKT.
A randomised prospective comparison of percutaneous endoscopic
gastrostomy and nasogastric tube feeding after acute dysphagic
stroke. BMJ 1996; 312: 1316.
Kasprisin AT, Clumeck H, Nino-Murcia, M. The efcacy of
rehabilitative management of dysphagia. Dysphagia 1989; 4: 4852.
Rosenbek JC, Robbins J, Fishback B, Levine RL. Effects of thermal
application on dysphagia after stroke. J Speech Hear Res 1991; 34:
125768.
Sukthankar SM, Reddy NP, Canilang EP, Stephenson L,
Thomas R. Design and development of portable biofeedback
systems for use in oral dysphagia rehabilitation. Med Eng Phys
1994; 16: 43035.
DePippo KL, Holas MA, Reding MJ, Mandel FS, Lesser ML.
Dysphagia therapy following stroke: a controlled trial. Neurology
1994; 44: 165560.
Anon. Recommendations on stroke prevention, diagnosis, and
therapy. Report of the WHO Task Force on Stroke and other
Cerebrovascular Disorders. Stroke 1989; 20: 140731.

http://neurology.thelancet.com Vol 5 January 2006

19
20

21

22
23
24
25
26

27

Warms T, Champion R, Mortensen L. The Paramatta hospitals

assessment of dysphagia. Aust Commun Q 1990; 11: 2526.
Warms T. The Paramatta hospitals assessment of dysphagia,
3rd edn. Sydney, Australia: Westmead Hospital and Community
Health Services, 1998.
Morgan A, Ward E, Murdoch B. Clinical progression and outcome
of dysphagia following paediatric traumatic brain injury:
a prospective study. Brain Inj 2004; 18: 35976.
Burn JP. Reliability of the modied Rankin scale. Stroke 1992;
23: 438.
Collin C, Wade DT, Davis S, Horne V. The Barthel ADL index:
a reliability study. Int Disabil Stud 1988; 10: 6163.
Basri H, Asman R. Predictors of in-hospital mortality after an acute
ischaemic stroke. Neurol J Southeast Asia 2003; 8: 58.
Lee AH, Somerford PJ, Yau KKW. Factors inuencing survival
after stroke in Western Australia. Med J Aust 2003; 179: 28993.
Thrift AG, Dewey HM, Macdonell RA, McNeil JJ, Donnan GA.
Stroke incidence on the east coast of Australia: the North East
Melbourne Stroke Incidence Study (NEMESIS). Stroke 2000;
31: 208792.
Ng WK, Goh KJ, Geiroge J, et al. A comparative study of stroke
subtype between Asian and Causcasians in two hospital based
stroke registries. Neurol J Southeast Asia 1988; 3: 1926.

37