Lung

DOI 10.1007/s00408-016-9929-5

Respiratory Muscle Assessment in Acute Guillain–Barré

Syndrome
S. Walterspacher1,3,5 • A. Kirchberger1 • J. Lambeck2 • D. J. Walker1,3,5 •
A. Schwörer1 • W. D. Niesen2 • W. Windisch1,3 • F. Hamzei2,4 • H. J. Kabitz1,5

Received: 24 April 2016 / Accepted: 2 August 2016

Ó Springer Science+Business Media New York 2016

Abstract Conclusion SnPna was the only parameter that correlated

Purpose Guillain–Barré Syndrome (GBS) is a life-threat- with MRC-SS, while the current gold standard of spirom-
ening disease due to respiratory muscle involvement. This etry measurement did not.
study aimed at objectively assessing the course of respi-
ratory muscle function in GBS subjects within the first Keywords Diaphragm
Respiratory muscle strength

week of admission to an intensive care unit. Intensive care
Sniff nasal pressure
Guillain–Barré
Methods Medical Research Council Sum Score (MRC- Syndrome
Acute Inflammatory Demyelinating
SS), vigorimetry, spirometry, and respiratory muscle Polyneuropathy (AIDP)
Vital capacity
function tests (inspiratory/expiratory muscle strength:
PImax/PEmax, sniff nasal pressure: SnPna) were assessed Abbreviations
twice daily. GBS Disability Score (GBS-DS) was assessed ANOVA One-way analysis of variance
once daily. On days one (d1) and seven (d7), blood gases CMAP Compound muscle action potential
and twitch mouth pressure during magnetic phrenic nerve GBS Guillain–Barré Syndrome
stimulation (Pmo,tw) were additionally evaluated. GBS-DS Erasmus GBS Disability Score
Results Nine subjects were included. MRC-SS, vigorime- MRC-SS MRC Sum Score
try, PImax, and SnPna increased between d1 and d7. GBS- P0.1 Respiratory drive
DS, spirometry and Pmo,tw remained unaltered. Only PEmax Global maximal expiratory muscle strength
SnPna correlated closely with the MRC-SS on both d1 PImax Global maximal inspiratory muscle strength
(r = 0.77, p = 0.02) and d7 (r = 0.74, p = 0.02). Pmo,tw Twitch mouth pressure
SD Standard deviation
& S. Walterspacher
SnPna Sniff nasal pressure
stephan.walterspacher@glkn.de VC Vital capacity
1
Clinic for Pneumology, Department of Internal Medicine,
University Hospital Freiburg, Freiburg, Germany
Introduction
2
Department of Neurology, University Hospital Freiburg,
Freiburg, Germany
Subjects with Guillain–Barré Syndrome (GBS), a periph-
3
Department of Pneumology, Kliniken der Stadt Köln gGmbH eral neuropathy with acute onset and mostly rapidly
Cologne, University of Witten/Herdecke, Witten, Germany
evolving skeletal muscle weakness, are at great risk of
4
Section of Neurological Rehabilitation, Hans Berger developing acute hypercapnic respiratory failure with up to
Department of Neurology, Jena University Hospital, Jena,
30 % demanding mechanical ventilation [1, 2]. This is
Germany
5
mainly attributed to hypoventilation, insufficient airway
Department of Pneumology, Cardiology, Intensive Care
protection, and limited secretion clearance [3]. Monitoring
Medicine, Academic Teaching Hospital University Freiburg,
Klinikum Konstanz, Luisenstrasse 7, 78464 Constance, of respiratory function is mainly performed by assessing
Germany vital capacity (VC), while ventilatory insufficiency is

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considered by a drop of 20 ml/kg VC or a decline of more
than 20 % of VC [1, 4]. Other monitoring techniques
include technically demanding electrophysiological
assessment of phrenic nerve function or the monitoring of
demyelination of peripheral nerves [4].
Neurophysiological function is commonly assessed by
established multifactorial scoring systems like the Erasmus
GBS Disability Score (GBS-DS) [5] and Medical Research
Council Sum Score (MRC-SS) [6]. However, both estab-
lished scoring systems do not assess respiratory function as
a specific item. Furthermore, lung function parameters are
considered not a sensitive tool for estimation of dooming
mechanical ventilation [4].
Hypercapnic respiratory failure is attributed to a failure
of the respiratory muscle pump, mainly the diaphragm as
its main component [7]. Current practice of respiratory
muscle function assessment in GBS however is either only
a surrogate of respiratory muscle function (i.e., spirometry)
or technically too demanding for everyday application
(e.g., electrophysiological measures). Yet, there are several
ways of assessing respiratory muscle function by applying
volitional and nonvolitional techniques [8]. These tech-
niques include the measurement of respiratory drive (P0.1),
global maximal inspiratory/expiratory muscle strength
(PImax/PEmax), sniff nasal pressure (SnPna), and nonvoli-
tionally assessed twitch mouth pressures (Pmo,tw). This
study aimed to assess respiratory muscle function using
established techniques to (a) analyze which technique best
predicts the course of respiratory muscle function in sub-
jects with GBS within the first week after the diagnosis and
to (b) evaluate its correlation to established neurophysio-
logical scoring systems.
Materials and Methods
The study design has been approved by the Institutional
Ethics Committee of the University Hospital Freiburg,
Germany and was performed in accordance with the ethical
standards laid down in the Declaration of Helsinki [9]. All
subjects proclaimed their written informed consent.
Subjects
Subjects were consecutively recruited from the Department
of Neurology at the University Hospital Freiburg, Ger-
many. They were included after clinical and neurophysio-
logical confirmation of GBS according to national
recommendations including electrodiagnostic studies of
peripheral nerves [10]. Subjects with a systemic infection
(C-reactive protein [ 5 mg/l), interstitial lung disease,
thorax deformation, obstructive pulmonary disorder, or
metal implantation were excluded. Baseline characteristics
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(anthropomorphic data, preceding gastrointestinal/respira-
tory infection, serological markers for Campylobacter
jejuni) were assessed at study entrance.
Study Set-Up
Within the first week after diagnosis, spirometry, periph-
eral (vigorimetry), and respiratory muscle function (i.e.,
P0.1, PImax, PEmax, SnPna), and the MRC-SS were assessed
twice and GBS-DS estimated once daily. On days one (d1)
and seven (d7), blood gas analysis and Pmo,tw were added
(see Fig. 1).
Neurophysiological functioning
MRC-SS comprises the summary score of 6 different
muscle groups measured bilaterally and assesses tetraple-
gia (0 points) up to normal functioning (60 points) [6]. The
GBS-DS interprets physical function and may vary from
normal (0 points) to death (6 points) [5].
Respiratory Assessment
Spirometry was performed in all participants (ZAN100Ò,
nSpire Health, Oberthulba, Germany) according to inter-
national recommendations [11, 12]. Ratings of perceived
exertion for dyspnea were assessed by the modified Borg
Scale [13]. Blood gases (cobas b221Ò, Roche Diagnostics,
Grenzach-Wyhlen, Germany) were measured from the
arterialized earlobe.
Respiratory muscle function was assessed according to
current recommendations [8, 14] using standardized
spirometry devices (Magnetic Shutter, ZAN100 and
ZAN400, nSpire Health GmbH, Oberthulba, Germany):
P0.1 after 0.1 s following inspiration during resting
breathing; global respiratory muscle function as repre-
sented by PImax/PEmax from residual volume/total lung
capacity, respectively; SnPna from functional residual
capacity. Pmo,tw was measured during bilateral anterior
magnetic phrenic nerve stimulation (Magstim 2002Ò,
Magstim, Whitland, UK) using an automated triggering
technique [15]. Peripheral muscle function was estimated
by hand-grip force (Martin Vigorimeter, Gebrueder Martin
GmbH, Tuttlingen, Germany).
Statistics
Statistical analysis was performed using SigmaStatÒ 3.5
(Systat Software, Chicago, Illinois, USA) and SigmaPlotÒ
10.0 (Systat Software, Chicago, Illinois, USA) for graphi-
cal presentation. Graphics were created using Microsoft
Word (Fig. 1) and SigmaPlot (Fig. 2).
Data were analyzed using the Kolmogorov–Smirnov test
for normal distribution prior to further statistical
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Fig. 1 CONSORT flow chart of
the study set-up. MRC-SS,
Medical Research Council Sum
Score; GBS-DS, Guillain–Barrè
Syndrome Disability Score;
P0.1, respiratory drive; PImax,
maximal static inspiratory
mouth pressure; PEmax,
maximal static expiratory mouth
pressure; SnPna, sniff nasal
pressure; Pmo,tw,
diaphragmatic twitch mouth
pressure
calculations. Normally distributed data are presented as
mean ± standard deviation (SD), and non-normally dis-
tributed data are provided as median with interquartile
ranges. Statistical significance was set at p \ 0.05 and
corrected for multiple corrections (Bonferroni correction).
The unpaired t test (normally distributed data) or Mann–
Whitney rank-sum test (nonnormally distributed data) was
used for comparing data from d1 and d7. For repeated
measurements, one-way analysis of variance (ANOVA)
was used; post hoc analysis was performed using the
Holm–Sidak test. Correlations between tests were evalu-
ated with Pearson product moment correlation. Linear
regression was also applied for the analysis of prediction.
Results
Nine subjects were included (six male) with a mean age of
56 ± 17 years and a body mass index of 26.9 ± 4.4 kg/
m2. All subjects were treated with plasmapheresis; two
subjects were treated twice due to an early relapse of
clinical symptoms. The first measurement was performed
within three days (range 0–7 days) from the first symptom
onset. Seven subjects described previous gastrointestinal
infections.
Subjects were hospitalized for 21 days (range
14–41 days). No subject needed mechanical ventilation, as
defined by the decision of the neurological intensive care
physician within the first week of in-hospital treatment or
the clinical follow-up measurement at week 12 after study
enrollment.
Neurophysiological function was assessed according to
the study protocol by the GBS-DS and MRC-SS (see
Table 1). Nerve conduction studies of peripheral nerves
revealed in all patients prolonged distal motor latencies and
pathological F-waves. Lung function parameters as asses-
sed according to the study protocol (Fig. 1) are presented in
Table 2. Respiratory muscle assessment is presented in
Table 3. Blood gases were assessed at d1 and d7 without
significant differences (see Table 4).
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Fig. 2 Regression analysis of sniff nasal pressure (SnPna) with the Medical Research Council Sum Score (MRC) sum score on day 1 and day 7

Table 1 Neurophysiological functioning as assessed by the GBS Regression analysis of vital capacity (VC) to the MRC-
Disability Score (GBS-DS) and MRC Sum Score (MRC-SS)
SS on d1 (r2 = 0.07; p = 0.5) and d7 (r2 = 0.11;
GBS-DS MRC-SS p = 0.78) revealed no association between both parame-
Day 1 3.1 (1.4) 38.6 (18.3) ters. Only SnPna presented a close and significant positive
Day 2 early* 3.4 (1.2) 38.5 (19.9)
correlation with the MRC-SS (Fig. 2). No correlations
Day 2 late* 38.1 (20.1)
were found for the GBS-DS and the other study
parameters.
Day 3 early* 3.4 (1.2) 39.8 (16.5)
Day 3 late* 39.4 (17.8)
Day 4 early* 3.4 (1.1) 42.0 (17.1)
Discussion
Day 4 late* 42.0 (17.1)
Day 5 early* 3.5 (1.1) 39.5 (16.4)
This study assessed respiratory muscle function by differ-
Day 5 late* 41.1 (18.9)
ent techniques in subjects during the acute stage of GBS.
Day 6 early  3.4 (1.2) 47.6 (11.9)
The main finding is that only SnPna presented a close
Day 6 late* 40.4 (19.2)
correlation with neurophysiological functioning measured
Day 7 3.4 (1.1) 42.3 (16.3)
with the MRC-SS. The current standard for assessment of
p 0.2 0.04
respiratory functioning is measurement of VC which did
day 1 versus day 7
not show any correlation with neurophysiological scores.
p 0.27 0.08
RM-ANOVA
Electrophysiological Assessment
 
* n = 8; n=7
Electrophysiological assessment appears as a feasible
P0.1 and vigorimetry revealed that there is no statistically tool—yet technically demanding—for estimation of
significant difference for both parameters within the study mechanical ventilation, especially in a specialized neuro-
period. SnPna presented a statistically significant differ- logical intensive care unit [16, 17]. Nerve conduction
ence with an increase from 5.2 ± 2.2 to 7.1 ± 2.0 kPa studies of the phrenic nerve showed that latency or duration
(p \ 0.001). Blood gas analysis showed normal values for of the compound muscle action potential (CMAP) was
all parameters assessed. However, there was a statistically correlated with the need for mechanical ventilation, while
significant difference for pH (d1: pH 7.4 ± 0.03 vs. d7: pH CMAP amplitude and area under curve were associated as
7.45 ± 0.04; p = 0.047). indices of respiratory muscle strength [17]. In the study by

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Table 2 Lung function parameters within the first week of treatment

FEV1 (l/s) FEV1 (%pred) VC max (l) VC max (%pred) Tiffeneau (FEV1/IVC) PEF (l/min) PEF (%pred)

Day 1 2.3 (1.0) 76.4 (25.9) 3.6 (1.4) 90.8 (23.3) 72.3 (17.9) 5.2 (1.8) 70.9 (22.3)
Day 2 early* 2.6 (1.4) 75.3 (32.3) 3.4 (1.4) 85 (24.1) 72.2 (20.5) 5.2 (2.3) 63.7 (28.3)
Day 2 late 2.5 (1.3) 79.4 (32.6) 3.4 (1.4) 85.2 (32.3) 72.9 (11.3) 5.3 (2.4) 67.6 (25)
 
Day 3 early 2.4 (1.0) 80.2 (28.9) 3.3 (1.1) 86.5 (26.0) 70.5 (12.4) 5.7 (2.4) 73.2 (27.3)
Day 3 late* 2.3 (1.0) 78.4 (31.3) 3.2 (1.1) 86.6 (25.5) 73.1 (19.2) 5.4 (2.3) 73.9 (26.8)
Day 4 early 2.5 (1.1) 78.7 (27) 3.5 (1.3) 87.7 (25.8) 70.8 (14.5) 5.4 (1.8) 69.6 (21)
Day 4 lateà 2.3 (1.3) 68.2 (24.3) 3.4 (1.2) 80 (17.1) 71.3 (23.1) 5.1 (1.8) 63.7 (20.8)
Day 5 early* 2.6 (1.3) 78.3 (26.9) 3.3 (1.2) 85.8 (24.6) 77.6 (15.7) 4.7 (1.9) 63.1 (23.4)
Day 5 late* 2.5 (1.2) 76.5 (27.2) 3.3 (1.5) 80.6 (26.1) 73.1 (13) 5.2 (2.6) 65.4 (30.5)
à
Day 6 early 2.9 (1.1) 90.2 (17.9) 3.6 (1.3) 93.3 (20.1) 80.6 (6.7) 6.1 (2.4) 78.9 (21.9)
Day 6 late* 2.7 (1.3) 80.1 (25.4) 3.4 (1.4) 82.6 (22.2) 74.8 (13.2) 5.6 (2.3) 70.3 (23.8)
Day 7 2.6(1.0) 83.3 (23.5) 3.7 (1.2) 93.0 (23.3) 70.3 (11.8) 5.5 (1.7) 72.9 (20.6)
p 0.48 0.16 0.79 0.69 0.61 0.55 0.42
(day 1 versus day 7)
p 0.17 0.37 0.79 0.73 0.86 0.84 0.76
RM-ANOVA
FEV1 forced expiratory volume in 1 s, VC vital capacity, PEF peak expiratory flow, %pred % predicted
  à
* n = 8; n = 7; n=6

Table 3 Respiratory muscle assessment

P0.1 (kPa) PImax (kPa) PEmax (kPa) SnPna (kPa) Pmo,tw (kPa) t-max (s) vigorimetry (kPa)

Day 1 0.2 (0.1) 5.8 (1.7) 6.9 (5.0) 5.2 (2.2) 0.6 (0.3) 139.4 (14.0) 44.3 (40.6)
Day 2 early* 0.2 (0.1) 6.8 (1.8) 7.9 (5.3) 5.3 (2.0) – – 43.9 (43.3)
Day 2 late* 0.2 (0.1) 6.0 (2.0) 7.7 (4.9) 5.9 (1.8) – – 48.9 (42.2)
Day 3 early  0.2 (0.0) 6.4 (2.5) 8.9 (7.3) 5.2 (1.8) – – 46.5 (55.4)
Day 3 late* 0.2 (0.1) 6.3 (2.3) 8.6 (5.5) 6.1 (2.0) – – 53.8 (50.4)
Day 4 early 0.2 (0.1) 6.5 (2.1) 8.0 (5.6) 6.3 (1.9) – – 59 (48.3)
Day 4 lateà 0.3 (0.1) 5.9 (2.0) 7.7 (7.1) 5.8 (1.9) – – 57.6 (47.1)
Day 5 early* 0.2 (0.1) 6.2 (2.7) 6.1 (2.9) 6.3 (2.3) – – 44.1 (28.9)
Day 5 lateà 0.3 (0.1) 6.6 (3.0) 8.4 (6.3) 6.5 (2.2) – – 55.7 (44.6)
Day 6 earlyà 0.2 (0.1) 7.5 (2.1) 8.8 (4.9) 7.6 (1.7) – – 74.4 (40.2)
Day 6 late* 0.3 (0.1) 6.3 (2.6) 7.5 (5.6) 6.6 (1.8) – – 59.1 (52)
Day 7 0.2 (0.1) 7.2 (2.5) 7.7 (4.9) 7.1 (2.0) 0.8 (0.2) 148.6 (11.7) 59.8 (49.5)
p 0.1 0.02 0.33 0.01 0.14 0.13 0.14
day1 versus day7
p \0.001 0.07 0.34 \0.001 – – 0.003
RM-ANOVA
Pmo,tw was assessed in n = 5 subjects
  à
* n = 8; n = 7; n=6
P0.1, respiratory drive; PImax, maximal static inspiratory mouth pressure; PEmax, maximal static expiratory mouth pressure; SnPna, maximal sniff
nasal pressure; Pmo,tw, twitch mouth pressure; t-max, time to pressure maximum following Pmo,tw; d1, day 1; d7, day 7

Zifko et al. [17] diaphragmatic dysfunction could be The phrenic nerve conduction and CMAP presented a
diagnosed in 88 % of GBS subjects, when electrophysio- high sensitivity (of 100 %) in predicting respiratory failure,
logical phrenic studies are performed. but only a distinct part of the respiratory pump (i.e., the

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Table 4 Blood gas parameters
pH
at day 1 and day 7
Day 1 7.3 (0.03)
Day 7 7.45 (0.04)
p 0.05
day 1 versus day 7
PaO2, arterial pressure of oxygen; PaCO2, arterial pressure of carbon dioxide; HCO3-, bicarbonate; BE,
base excess
diaphragm as its main component) was investigated;
therefore their specificity were low [17]. This is in line with
the current findings. The nonvolitionally assessed
diaphragmatic strength (Pmo,tw) did not correlate with
neurophysiological markers while volitionally assessed
parameters of respiratory muscle strength (SnPna) showed
a close correlation. It becomes evident, that respiratory
muscle function in its entirety has to be assessed by easier
means.
Respiratory Muscle Tests
There are several ways to analyze respiratory muscle func-
tioning [8, 18], even in subjects with critical illness and during
intensive care treatment [19]. Volitional techniques include
maximal static inspiratory and expiratory mouth pressures
(PImax/PEmax), as well as sniff nasal pressure (SnPna). Non-
volitional techniques include technically demanding magnetic
or electrical stimulation of the phrenic nerve and measurement
of mouth or transdiaphragmatic pressures.
PImax and SnPna are established in chronic neuromus-
cular disorders as a testing tool for respiratory muscle
function [20, 21]. In a previous study, PImax and VC have
been evaluated in GBS subjects. PImax and VC were
comparable in their sensitivity in the detection of respira-
tory muscle failure [22]. Nonetheless, VC is not specific for
the diagnosis of respiratory muscle weakness and is
impaired in various pulmonary disorders [8]. Especially in
subjects with milder disease, VC is considered less sensi-
tive than PImax/PEmax measurements [23]; this is presum-
ably due to the curvilinear relation of VC and maximal
inspiratory pressures [24].
The current findings confirm and extend previous
investigations. SnPna is considered a more natural
maneuver, due to its dynamic execution compared to static
pressure measurements such as PImax [25]. It is a hand-free
technique at the open airways occluding just one nostril,
leaving one nostril and the mouth open [8]; therefore
avoiding the alarming feeling of totally occluded airways
in breathless subjects as in PImax measurements. It is
considered to be more easily adopted and easier performed
by inexperienced subjects and reflects more closely
diaphragmatic pressure than PImax [8, 26]. SnPna
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PaO2 (mmHg) PaCO2 (mmHg) HCO3- (mmol/l) BE (mmol/l)
76.7 (18.6) 39.2 (3.7) 24.1 (3.7) -0.5 (2.9)
79.3 (11.2) 35.4 (5.4) 23.2 (3) -0.1 (3)
0.86 0.17 0.64 0.87
presumably activates the neuromuscular system of the
respiratory muscles more completely than PImax [27] and is
assumed to be the main determinant of VC in subjects with
neuromuscular disorders [28]. Especially in subjects with
bulbar involvement, spirometry and PImax assessment may
lead to false readings due to air leakage [27]. In a study
with subjects suffering from amyotrophic lateral sclerosis,
SnPna was the best predictor for intubation or tra-
cheostomy and more sensitive to minimal changes in res-
piratory muscle function, when compared to vital capacity
measurements. SnPna was also more reliable in subjects
with severe bulbar affection since air leaks at the mouth are
avoided [29]. Furthermore, SnPna was a more sensitive
marker for hypercapnia in neuromuscular disorders than
PImax [30, 31]. However, in this study, blood gas parame-
ters were all within normal ranges and no patient demanded
mechanical ventilation. Therefore, further studies have to
attempt the determination of a threshold of SnPna reduc-
tion at which respiratory failure is imminent.
Neurophysiological Scores
Most studies and guidelines regarding GBS do not imple-
ment dedicated tests for respiratory muscle function, as
proposed by international respiratory societies [8] and
mainly apply surrogate techniques such as the assessment
of VC [4, 32]. However, VC measurement has long been
criticized as an insufficient test to predict mechanical
ventilation [8, 33]. Additionally, neurophysiological scores
were evaluated in acute stages of GBS and the MRC-SS
appeared to predict mechanical ventilation more suffi-
ciently than GBS-DS [34]. These previous findings are in
line with the current findings, since only the MRC-SS
significantly correlated with SnPna as a dedicated param-
eter of respiratory muscle strength and surrogate of
diaphragmatic function. This presumably reflects the
quality of the MRC-SS and its association with SnPna,
evaluating physical functioning more specifically than
GBS-DS or VC measurements.
In this study, SnPna has proven to be an easy to apply
technique, sensitive enough to detect changes in respiratory
muscle strength and to correlate with neurophysiological
scores such as the MRC-SS. However, previous studies in
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subjects with several neuromuscular disorders have shown
that the limits of agreement between PImax and SnPna are
wide, indicating that SnPna and PImax are not inter-
changeable but should be considered complementary [35].
The combination of both tests leads to a relative reduction
of false positive diagnosis of respiratory muscle weakness
by 19.2 % in healthy subjects [18]).
Critique of Methods
The following methodological limitations of the current
study need to be addressed. First, the sample size was
small, but due to the study design and complex twice daily
assessment of the subjects, no more subjects could be
included within the study period.
Second, the study population did not include subjects
that entered mechanical ventilation or with hypercapnia.
Therefore, cut-off values for SnPna indicating the need for
mechanical ventilation cannot be determined; this should
be subject of further studies. No subjects turned out to be
hypercapnic and/or needed mechanical ventilation, which
is surprising, because according to GBS-DS and MRC
scoring at admission, the included subjects were at inter-
mediate risk for respiratory failure [36]. It is suggested that
the aggressive treatment of GBS (with plasmapheresis and/
or intravenous immunoglobulin) was capable of preventing
hypercapnic failure in these subjects.
Third, Pmo,tw as a gold standard for respiratory muscle
assessment was not assessed on every study day [8].
However, due to the demanding procedures of Pmo,tw
assessment and high technical effort in generating these
measurements, daily measurements could not be obtained.
Fourth, the study time frame of 1 week might be too
short in order to adequately address respiratory muscle
affection of GBS. A longer study period might show a
better correlation with other parameters during disease
progression. However, for our subjects, a longer study
period would not have a greater influence on the current
results, since none of the subjects developed respiratory
failure demanding mechanical ventilation despite respira-
tory muscle weakness.
Conclusion
This prospective study revealed for the first time that the
SnPna is well associated with neurophysiological function-
ing scores (MRC-SS) in subjects suffering from acute GBS.
The current standard procedure of estimating respiratory
muscle function in GBS with spirometry in contrast did not
show any correlation with respiratory muscle functioning or
neurophysiological scores. SnPna might have the potential
to replace spirometry assessment in GBS subjects.
Acknowledgments All participants are acknowledged for their time
and effort.
Funding This work was supported by a research grant from the
German Research Foundation DFG (Deutsche Forschungsgemein-
schaft), Bonn, Germany [KA 2992/2-1].
Compliance with Ethical Standards
Conflict of interest The authors declare that they have no conflict of
interest.
Ethical Approval All procedures performed in studies involving
human participants were in accordance with the ethical standards of
the institutional and/or national research committee and with the 1964
Helsinki declaration and its later amendments or comparable ethical
standards.
Informed Consent Informed consent was obtained from all indi-
vidual participants included in this study.
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