Sleep and Psychiatric Abnormalities in Gullian Barré Syndrome

Download as pdf or txt
Download as pdf or txt
You are on page 1of 7

Bahnasy et al.

The Egyptian Journal of Neurology, Psychiatry and Neurosurgery


(2018) 54:5
The Egyptian Journal of Neurology,
https://doi.org/10.1186/s41983-018-0007-1 Psychiatry and Neurosurgery

RESEARCH Open Access

Sleep and psychiatric abnormalities in


Gullian Barré Syndrome
Wafik Said Bahnasy1*, Yasser Abo Elfotoh El-Heneedy1, Ahmed Mohamed El-Shamy1, Marwa Yassin Badr1,
Reham Ahmed Amer2 and Ibrahim Salah Eldeen Ibrahim3

Abstract
Background: The sensori-motor manifestations of Guillain Barré Syndrome (GBS) are usually severe enough to mask
the psychiatric and sleep problems which are in need for more attention for better functional outcome.
Methods: This study was performed on 20 GBS patients and 10 healthy controls. Patients were evaluated initially
before immunotherapy using the Overall Disability Sum Score (ODSS), Neuropathy Pain Scale (NPS), Hamilton
Anxiety Scale (HAS), Montgomery–Åsberg Depression Rating Scale (MADRS) and one-night polysomnography (PSG)
followed by the multiple sleep latency test (MSLT) to evaluate the mean sleep latencies. Reevaluation was done
using the same parameters 1 month after completing immunotherapy.
Results: The study showed significant increase in HAS in GBS patients which were positively correlated with the
degree of motor disability. The mean sleep latencies of MSLT were significantly shortened and PSG showed
shortening of the total sleep time, sleep efficiency, lowest O2 saturation and pulse transit time with increased wake
after sleep onset, sleep stage transition index, apnea hypopnea index, desaturation index, arousal index, snore index
and periodic limb movement index. One month after immunotherapy, the anxiety symptoms and sleep
abnormalities showed non-significant improvements which were not correlated with the improvements in the
sensori-motor manifestations.
Conclusions: GBS patients usually have sleep and psychiatric abnormalities which may take longer time to improve
than the sensori-motor manifestations. So, they need more attention in the management protocol for early
patients’ independence and return to usual daily activities.
Keywords: Guillain Barré Syndrome, Multiple sleep latency test, Polysomnography, Hamilton anxiety scale, MADRS

Background Gullian Barré Syndrome is predominantly demyelinating


Guillain Barré Syndrome (GBS) is an acute monophasic in Europe and the USA and predominantly axonal in
poly-radiculo-neuritis manifested by motor deficits, Asia, North Africa, and South America (Willison et al.
diminished reflexes, sensory dysfunction, and sometimes 2016; van den Berg et al. 2014).
cranial nerve affection (Wakerley et al. 2014). The Guillain Barré Syndrome patients may experience psychi-
annual incidence of GBS is about 1–2 per 100,000, 30% atric manifestations in the form of anxiety and depressive
of patients may need assisted ventilation, and 2–5% die symptoms which contribute to their slow recovery
of complications. Recovery from GBS usually takes long (Darweesh et al. 2014). They also experience sleep problems
time with most of patients experience good motor out- in the form of REM behavior disorders and sleep apneas
comes and return to the usual daily activities in up to due to increased upper airway resistance and weakness of
3 years from the onset with 20% still have residual the respiratory muscles and centrally due to respiratory
disabilities (Meena et al. 2011; Alshekhlee et al. 2008). chemoreceptors hypo-responsiveness (Peralta et al. 2006).

* Correspondence: [email protected] Aim of the work


1
Department of Neuropsychiatry, Faculty of Medicine, Tanta University, Tanta
31527, Egypt Was to assess sleep and psychiatric abnormalities in GBS
Full list of author information is available at the end of the article patients, their relations to the severity of sensori-motor
© The Author(s). 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and
reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to
the Creative Commons license, and indicate if changes were made.
Bahnasy et al. The Egyptian Journal of Neurology, Psychiatry and Neurosurgery (2018) 54:5 Page 2 of 7

manifestations, and the possibility of their spontaneous parameter measuring excessive daytime sleepiness). PSG
recovery after GBS immunotherapy. and MSLT were performed by a Somon Medics Gmbh
(Am SonnenstuhL63, D-97236 Rander Sacker, Germany,
Methods Type: SOMNO screen™plus, SN: 4259, kw45: 2014). The
The present study was conducted on 20 adult GBS patients PSG included EEG channels montages (O1/A2, C3/A2, C4/
fulfilling the level 1 or 2 diagnostic certainty of The Brighton A1 and O2/A1), electrooculography (LOC-A1/A2 and
Criteria (Goodfellow and Wilson 2016) attending The ROC-A1/A2), surface tibial and submental EMG, and
Neuropsychiatry Department, Tanta University Hospitals, in modified V2 lead ECG. Thermal airflow sensors (thermis-
the period from 1st of April to the end of December 2016. tor) were used for nasal and oral signals, and microphone
Ten healthy control subjects matching the patient’s age, sex, was applied for tracheal sounds assessment. Chest and
and body mass index (BMI) were also included. Six patients abdominal efforts were measured by dual thoracoab-
needed cerebrospinal fluid examination, who showed the dominal RIP (respiratory inductance plethysmography)
cyto-albuminous dissociation needed for diagnostic cer- belts. PSG parameters were scored according to The
tainty. Neurophysiology was done to all patients 2–3 weeks American Academy of Sleep Medicine Scoring Man-
after the onset of symptoms to confirm the diagnosis and ual, 2012 (Grigg-Damberger 2012).
fulfill The Brighton Criteria. The neurophysiology included One month after completing immunotherapy, patients
bilateral motor conduction studies and F-wave latencies for were reassessed using the same parameters (HAS and
each of median and ulnar nerves. Bilateral motor conduc- MADRS, PSG and MSLT) to evaluate the degree of im-
tion studies and H-wave latencies for common peroneal and provements in each and correlate them with the degrees
posterior tibial nerves. At the same time, bilateral sensory of sensori-motor changes (ODSS and NPS).
conduction studies for each of median, ulnar, and Statistical analysis was conducted using the ANOVA
sural nerves were done (sural sparing if present is and Tukey’s tests. Correlation analysis was performed
confirmatory for GBS). using Pearson’s correlation test. P value less than 0.05
Exclusion criteria included GBS patients in impending was considered statistically significant.
need of assisted ventilation who spirometer forced vital cap-
acity less than 20 ml/kg, patients with chronic respiratory or Results
cardiac problems, chronic pain, BMI≥ 28 kg/m2, advanced The study included 20 GBS patients aged 39.05 ± 11.3 years,
metabolic or endocrinal disorders, drugs affecting sleep 13 males (65%) and 7 females (35%) with BMI 24.9 ±
intake, heavy smokers or history of psychiatric disorders. 2.4 kg/m2. Ten (50%) patients had history of upper
The study protocol was approved by The Research respiratory tract infection, 4 (20%) had gastroenteritis, and 6
Ethics Committee and Quality Assurance Unit, Faculty (30%) could not decide. The patients were admitted 12.8 ±
of Medicine, Tanta University. Participation was volun- 2.9 days following symptoms onset, and this relatively
tary, all participants received detailed information con- delayed admission in some patients was due to initial faulty
cerning the aims and possible risks of sharing in this diagnosis by family doctors and false impression of possible
research work, and an informed consent was obtained spontaneous recovery during early mild initial symptoms.
from all prior to the commencement in the study. Eighteen patients (90%) underwent plasmapheresis, and 2
Patients were submitted to GBS management protocol (10%) received intravenous immunoglobulin, and the mean
including 5–7 sessions of plasmapheresis (200–250 mL/kg time lapses between admission and the first session of
of plasma was exchanged over 2 weeks) or intravenous immunotherapy were 3.1 ± 1.1 days till immunotherapy
immunoglobulin (0.4 g/kg/dose for 5 doses in 5 consecu- became ready during which initial assessments were done.
tive days). In initial assessments, all patients had bilateral sym-
Patients were evaluated initially at the time of hospital metrical weakness both proximal and distal, absent or
admission and before immunotherapy using The Overall diminished deep reflexes mainly the ankle jerk; 5 (25%)
Disability Sum Score (ODSS) (Merkies et al. 2002) and patients had equivocal planter response; 4 (20%) had
The Neuropathy Pain Scale (NPS) (Jensen et al. 2006) to unilateral facial palsy; 3 (15%) had facial diplegia; and 3
assess the degree of motor and sensory manifestations (15%) had bulbar symptoms. Neurophysiological exam-
respectively. Psychiatric assessment was done using ination revealed that 15 (75%) patients had predomin-
Hamilton Anxiety Scale (HAS) and Montgomery– antly demyelinating, 2 (10%) patients had predominantly
Åsberg Depression Rating Scale (MADRS) for anxiety axonal neuropathy, and 3 (15%) patients had normal
and depressive symptoms severities (Maier et al. 1988; neurophysiology.
Williams and Kobak 2008). The ODSS and NPS were significantly higher in GBS pa-
All subjects were submitted to one-night polysomnogram tients compared to healthy control subjects (5.9 ± 0.8 and
(PSG) followed in the next day by multiple sleep latency 17.4 ± 8.3 versus 0.7 ± 0.8 and 9 ± 3.6 with p value < 0.0001
test (MSLT) to assess the mean sleep latencies (objective and 0.004 respectively). The HAS and MADRS were also
Bahnasy et al. The Egyptian Journal of Neurology, Psychiatry and Neurosurgery (2018) 54:5 Page 3 of 7

significantly higher in GBS patients than healthy control 92.5 ± 2.5, and 241.4 ± 13.2 respectively with p value <
subjects (25.9 ± 5.7 and 18.9 ± 10 versus 7.7 ± 2.2 and 7.4 ± 0.0001 for each). There were significant increases in
5.1 with p value < 0.0001 and 0.002 respectively) (Table 1). wake after sleep onset (WASO), sleep stage transition
The HAS and MADRS showed non-significant correl- index (SSTI), apnea hypopnea index (AHI), and desat-
ation with the rate of initial disease progression mea- uration index (DI) in GBS patients compared to healthy
sured by the onset-admission duration (p-values 0.439 control subjects (2.91 ± 0.59, 21.9 ± 6.5, 19.1 ± 7.8, and
and 0.965 respectively). 17.4 ± 7.3 versus 0.9 ± 0.3, 8.6 ± 1.6, 5.7 ± 5.5, and 6.2 ±
The study showed significant decrease in the mean 5.04 respectively with p value < 0.0001 for each). Sleep
sleep latencies of the MSLT in GBS patients compared architecture of GBS patients showed prolonged WASO
to control (11.8 ± 4 versus 16.6 ± 2.2 with p value 0.002). on the expense of shortened N2% and REM% of TST with
Polysomnography showed significant reduction in each nearly normal N1% of TST and relatively prolonged
of total sleep time (TST), sleep efficiency (SE), lowest O2 N3% of TST (19.6 ± 6.3%, 9.3 ± 3.8%, 8.1 ± 2.5%, and
saturation, and pulse transit time (PTT) in GBS com- 24.3.3 ± 3.2% respectively) (Fig. 1).
pared to healthy control subjects (5.3 ± 0.4, 62.6 ± 5.9, There was also significant increase in each of arousal
86.5 ± 2.9, and 184.6 ± 23.2 versus 7.3 ± 0.3, 86.4 ± 4.2, index (AI), snore index (SI), and periodic limb movement

Table 1 Comparison between Gullian Barré patients and control subjects at initial assessment
Patients Control ANOVA
Mean ± SD Mean ± SD f value p value
Overall Disability Sum Score Early 5.95 ± 0.82 0.7 0 ± 0.82 156.47 > 0.0001*
Late 4.15 ± 0.67 > 0.0001*
Neuropathy Pain Scale Early 17.35 ± 8.28 9.0 ± 3.59 10.09 0.004*
Late 9.15 ± 5.02 0.998
Hamilton Anxiety Scale Early 25.9 ± 5.7 7.7 ± 2.16 22.5 > 0.0001*
Late 21.15 ± 5.54 > 0.0001*
MADRS Early 18.9 ± 9.96 7.4 ± 5.08 6.74 0.002*
Late 15.55 ± 7.12 0.033*
Mean sleep latency of MSLT (min) Early 11.79 ± 3.97 16.64 ± 2.2 6.79 0.002*
Late 14.23 ± 3.45 0.185
Total sleep time (hours) Early 5.28 ± 0.43 7.29 ± 0.33 70.49 > 0.0001*
Late 5.64 ± 0.49 > 0.0001*
Wake after sleep onset (hours) Early 2.91 ± 0.588 0.85 ± 0.34 64.66 > 0.0001*
Late 2.53 ± 0.41 > 0.0001*
Sleep efficiency (%) Early 62.56 ± 5.93 86.38 ± 4.22 74.44 > 0.0001*
Late 67.53 ± 4.57 > 0.0001*
SSTI (No of sleep stages/h) Early 21.9 ± 6.51 8.6 ± 1.6 24.5 > 0.0001*
Late 19.74 ± 4.36 > 0.0001*
Apnea hypopnea index (/hour) Early 19.11 ± 7.75 5.67 ± 5.46 16.64 > 0.0001*
Late 18.2 ± 5.15 > 0.0001*
Pulse Transit Time (msec) Early 184.6 ± 23.2 241.4 ± 13.2 13.6 > 0.0001*
Late 232.3 ± 12.3 > 0.0001*
Arousal index (/hour) Early 37.6 5 ± 12.69 5.5 ± 2.63 33.64 > 0.0001*
Late 35.4 ± 10.98 > 0.0001*
Snore Index (/hour) Early 299.3 ± 142.25 29.1 ± 21.89 22.53 > 0.0001*
Late 234.45 ± 81.66 > 0.0001*
Periodic limb movements index (/hour) Early 46.35 ± 22.61 9.9 ± 3.66 13.29 > 0.0001*
Late 41.0 ± 18.92 > 0.0001*
Early after admission and before immunotherapy, Late 1 month after immunotherapy, MADRS Montgomery–Åsberg Depression Rating Scale, MSLT multiple sleep
latency test, SSTI sleep stage transition index
*Significant
Bahnasy et al. The Egyptian Journal of Neurology, Psychiatry and Neurosurgery (2018) 54:5 Page 4 of 7

Fig. 1 Sleep stages from total sleep time (TST) in a Gullian Barré Patient early after hospital admission (left) with marked prolongation of waking
after sleep onset (W) and shortening of each N2% and REM% of TST. One month after immunotherapy (right), the same patient showed mild
improvement of sleep architecture but still not reaching the normal values

index (PLMI) in GBS patients than control (37.7 ± 12.7, SSTI, AHI, DI, AI, SI, and PLM indices were signifi-
299.3 ± 142.3, and 46.4 ± 22.6 versus 5.5 ± 2.6, 29.1 ± 21.9, cantly higher in GBS patients with p value < 0.0001
and 9.9 ± 3.7 respectively with p value < 0.0001 for each) for each parameter (Table 1).
(Table 1) (Fig. 2). Sleep and REM latencies showed non- One month after immunotherapy, the GBS patients
significant difference between GBS patients and healthy revealed significant improvements in the ODSS and
control subjects. The studied GBS patients had no correl- NPS with p value 0.0001 and 0.001 respectively when
ation between the evaluated PSG parameters at the time compared with initial assessment. The HAS and
of admission and severities of motor disabilities as mea- MADRS showed non-significant changes with p value
sured by the ODSS (except SE which showed negative 0.22 and 0.398 respectively. The study also showed
correlation with ODSS) (Table 2). The PSG abnormalities that motor deficits measured by the ODSS were not
are more severe in those having cranial nerve affection. correlated with the patients’ age, HAS, MADRS, mean
The study showed that the initial ODSS was positively sleep latencies of the MSLT, and other examined PSG
correlated with the HAS, WASO, and SI and negatively parameters (Table 3). At the same time, the ODSS
correlated with SE and had no correlations with improvement was 1.8 ± 0.8 which was not correlated with
MADRS, MSLT, and other PSG parameters (Table 2). At the degree of HAS and MADRS improvements (3.05 ± 1.36
the same time, the initial HAS measured at the time of and 3.1 ± 3.5 with p values 0.303 and 0.638 respectively).
admission was positively correlated with NPS, MADRS, Regarding sleep architecture, GBS patients showed
WASO, AHI, and DI and negatively correlated with non-significant changes in each of the mean latencies of
MSLT and SE, and had no correlation with TST, SSTI, MSLT, SSTI, AHI, DI, AI, and PLM indices. Each of
AI, SI, and PLMI (Table 2). TST, WASO, SE, lowest O2 saturation, and SI showed
The study showed that comparing GBS patients 1 month mild significant improvement with p value 0.034, 0.014,
after immunotherapy with the initially evaluated healthy 0.01, 0.042, and 0.034 respectively.
control subjects’ data revealed non-significant difference
regarding NPS and mean latencies of MSLT with p value Discussion
0.99 and 0.185 respectively. Each of ODSS, HAS, and Guillain Barré Syndrome is an acute monophasic post-
MADRS showed significant increase in GBS patients than infectious immune-mediated peripheral neuropathy with
control with p values < 0.0001, < 0.0001, and 0.033 sensory disturbances, motor weakness, and diminished
respectively. At the same time, PSG showed signifi- or absent reflexes with or without cranial nerve affec-
cant reduction in each of TST, SE, and lowest O2 sat- tion. Patients with GBS usually need prolonged hospital
uration in GBS compared to healthy control subjects stay and often experience anxiety and sleep disturbances
(p values < 0.0001 for each). Wake after sleep onset, (Karkare et al. 2013).

Fig. 2 Hypnogram of a Gullian Barré patient showing increased waking after sleep onset and sleep stage transition index with shortened rapid
eye movement sleep (R) and N2 non-rapid eye movement sleep (2)
Bahnasy et al. The Egyptian Journal of Neurology, Psychiatry and Neurosurgery (2018) 54:5 Page 5 of 7

Table 2 Correlations of the Overall Disability Sum Score and Hamilton Anxiety Scale with other studied parameters in Gullian Barré
patients at initial assessment
Early ODSS Hamilton Anxiety Scale
r p r p
Neuropathic Pain Scale 0.31 0.18 0.52 0.01*
Hamilton Anxiety Scale 0.50 0.024* – –
Montgomery–Åsberg Depression Rating Scale − 0.03 0.87 0.44 0.05*
Mean sleep latency of MSLT (min) 0.3 − 0.15 − 0.75 0.0001*
Total sleep time (hours) 0.40 0.07 − 0.37 0.1006
Wake after sleep onset (hours) 0.68 0.001* 0.97 < 0.0001*
Sleep efficiency (%) − 0.69 0.0007* − 0.89 < 0.0001*
Sleep stage transition index (/hour) − 0.15 0.51 0.22 0.34
Apnea hypopnea index (/hour) 0.44 0.046* 0.84 < 0.0001*
Arousal index (/hour) − 0.22 0.33 0.02 0.91
Snore Index (/hour) 0.55 0.0117* − 0.34 0.13
Periodic limb movements index (/hour) 0.17 0.45 − 0.01 0.93
Early ODSS Overall Disability Sum Score on admission, MSLT multiple sleep latency test
*Significant

This work studied the possible psychiatric and sleep higher among those lacking cranial nerve affection,
abnormalities in GBS patients. The study showed that milder disabilities, demyelinating neuropathies, younger
GBS is more common in middle-aged males and about ages, and lower CSF proteins. These results are in ac-
half of the cases had cranial nerve affection, and neuro- cordance with the work of González-Suárez et al. (2013)
physiology showed that most of the patients were and Fokke et al. (2014) who studied the predictors of
predominantly demyelinating motor neuropathy. The outcome in GBS patients and concluded that bad prog-
improvements in the sensori-motor manifestations were nosis is demonstrated among older-aged GBS patients,
severe motor deficits at onset, injured cranial nerves,
Table 3 Correlations of the Overall Disability Sum Score and and axonal lesion patterns in the neurophysiological
other studied parameters, 1 month after finishing immunotherapy examinations.
Overall Disability Sum Score after 1 month The study declared that after exclusion of cases with
r p severe motor disability, GBS patients experienced mod-
Patients’ ages 0.13 0.56
erate–severe anxiety and mild-moderate depressive
symptoms during the early phases of the disease before
Neuropathic Pain Scale 0.05 0.81
immunotherapy which were positively correlated with
Hamilton Anxiety Scale − 0.27 0.24 the degree of motor disability. Both anxiety and depres-
Montgomery–Åsberg − 0.11 0.62 sive symptoms were non-significantly correlated with
Depression Rating Scale
the rapidity of symptoms progression measured by the
Mean sleep latency of MSLT − 0.10 0.66 duration between symptoms onsets and admission times
(min)
which are possibly explained by the exclusion of GBS
Total sleep time (hours) − 0.02 0.92 patients with severe motor disabilities that may exhibit
Wake after sleep onset − 0.07 0.75 more rapid disease progression. These results are pass-
(hours)
ing with the work of Bernsen et al. (2010) who found a
Sleep efficiency (%) 0.08 0.72 high rate of anxiety among GBS patients in early disease
Sleep stage transition index 0.024 0.30 stages and attribute this to ICU admission, fear of need
(/hour) of assisted ventilation and haziness in the expectation
Apnea hypopnea index − 0.15 0.52 about the future prognosis, but on the contrary, they
(/hour)
found positive correlation with rapidity of disabilities
Arousal index (/hour) 0.07 0.76 possibly due to non-exclusion of those needed assisted
Snore Index (/hour) 0.09 0.69 ventilation who may have more rapid disease course.
Periodic limb movements − 0.013 0.95 Brousseau et al. (2005) went beyond these results,
index (/hour) and they found higher rate of anxiety, depressive
MSLT multiple sleep latency test symptoms, and brief reactive psychosis in GBS
Bahnasy et al. The Egyptian Journal of Neurology, Psychiatry and Neurosurgery (2018) 54:5 Page 6 of 7

patients than that in ICU-admitted patients for other indi- improve and may need treatment either pharmacologically
cations with near degree of disability and supposed that or by continuous positive airway pressure ventilation
psychiatric symptoms are parts of the clinical manifesta- (CPAP) to reduce the patient’s suffering. This observation
tions of GBS. is in accordance with that of Cochen et al. (2005) and
One month after immunotherapy, the patients showed Chokroverty (2003) who declared that GBS patients ex-
good recovery of the sensori-motor manifestations while hibit a lot of sleep abnormalities including REM behavior
the anxiety and depressive symptoms showed non- disorders, transitory hypocretin-1 transmission decrease,
parallel improvement which means that they need longer and sleep-disordered breathing which may need manage-
time, may not resolve spontaneously, and are in need of ment for earlier patients’ recovery and independence.
specific psychiatric treatment. These results agree with
Bernsen et al. (2010) who found psychological dysfunc- Limitations
tions in GBS patients persisting up to 1 year from the The limitations of this study are the small sample size
disease onset. Brousseau et al. (2005) advise the use of and the need for longer follow-up period which is
modest doses of specific serotonin reuptake inhibitors, intended to be overcame in a second phase of the study.
anticonvulsants, and supportive psychotherapy to ameli- Also, exclusion of GBS patients with impending respira-
orate the symptoms of anxiety and depression during tory failure is added to the study limitations.
rehabilitation of GBS patients for better prognosis and
earlier independence. Conclusion
Regarding the sleep assessment, the study showed EDS Sleep and psychiatric disturbances are common manifes-
in initial evaluation of GBS patients as evidenced by tations of GBS which are not proportional with the
shortened mean latencies of MSLT. This result agrees degree of motor disability and rapidity of progression.
with that of Gao et al. (2016) who found EDS in GBS These disturbances need special attention in the man-
patients through using the Pittsburgh Sleep Quality agement protocol for earlier patients' independence and
Index. Polysomnographic assessment during this stage better functional outcome.
showed marked prolongation of WASO on the expense
Abbreviations
of reduction in TST, decreased SE, and increased SSTI. AHI: Apnea hypopnea index; AI: Arousal index; BMI: Body mass index;
Sleep architecture showed shortened N2% and REM% of DI: Desaturation index; GBS: Guillain Barré Syndrome; HAS: Hamilton Anxiety
TST with nearly normal N1% and relatively prolonged Scale; MADRS: Montgomery–Åsberg Depression Rating Scale; MSLT: Multiple
sleep latency test; N2: Non-rapid eye movement sleep stage 2; NPS: Neuropathy
N3% of TST. The PSG abnormalities and EDS were pro- pain scale; ODSS: Overall disability sum score; PLMI: Periodic limb movement
portional with the severity of anxiety symptoms. These index; PSG: Polysomnogram; PTT: Pulse transit time; REM: Rapid eye movement;
results are partly going with the work of Cochen et al. SE: Sleep efficiency; SI: Snore index; SSTI: Sleep stage transition index; TIB: Total
in bed time; TST: Total sleep time; WASO: Wake after sleep onset
(2005) who found shortening and fragmentation of all
sleep stages in GBS patients. Acknowledgements
The study also showed increased AHI, DI, AI, and SI The work was carried out in Neuropsychiatry and Chest Departments, Faculty
of medicine, Tanta University.
with shortening of the PTT pointing to the presence of
mild–moderate obstructive sleep apnea (OSA) syndrome Authors’ contributions
in the studied patients especially those who had cranial WSB participated in the study idea, design, and patients’ collection and
performed statistical analysis, polysomnographic data analysis, references
nerve affection and bulbar symptoms. The OSA was collection, and manuscript writing and revision. YAH participated in the
mild–moderate in severity (AHI was 19.11 ± 7.75) pos- study design, patients’ collection, neurophysiological studying, and study
sibly due to exclusion of patients with severe motor def- revision. AMS participated in the patients’ collection, statistical analysis, and
manuscript writing and revision. MYB participated in the patients’ clinical
icit. These results agree with that of Chokroverty (2003) neuropathy scoring, follow-up of the patients and their registration, MSLT
who stated that chest wall and respiratory muscle fatigue interpretation, and follow-up of patients’ treatment schedule. RAA participated
with extension of the REM sleep hypotonia to affect the in the study design, psychological assessment of the patients, and control,
references collection, and manuscript revision. ISI participated in the study
respiratory muscles (the extra-ocular and respiratory design, patients’ chest evaluation, MSLT and PSG interpretation, and manuscript
muscles are normally not involved in the REM sleep revision. All authors read and approved the final manuscript.
hypotonia) may be the cause of OSA in GBS patients.
Ethics approval and consent to participate
Periodic limb movement index also showed significant
increase in early disease stages, and this result is also – The study protocol was approved by The Research Ethics Committee
passing with the work of Gao et al. (2016). and Quality Assurance Unit, Faculty of Medicine, Tanta University.
Participation was voluntary, all participants received detailed
Re-evaluation of the patients 1 month after immuno- information concerning the aims and possible risks of sharing in this
therapy showed mild improvement of MSLT and some research work and an informed consent was obtained from all prior
PSG parameters but still significantly impaired when com- to the commencement in the study.
– The URL: http://tqac.tanta.edu.eg/new-tqac/
pared with the control group which point to that sleep [email protected]
disturbances in GBS patients may take long time to – Approval Code: 30888/04/16
Bahnasy et al. The Egyptian Journal of Neurology, Psychiatry and Neurosurgery (2018) 54:5 Page 7 of 7

– Name of the PI: Wafik Said Kamel ElBahnasy. Wakerley BR, Uncini A, Yuki N. Guillain–Barré and Miller Fisher syndromes: new
– Name of the department: Neuropsychiatry. diagnostic classification. Nat Rev Neurol. 2014;10:537–44.
– Type of the research: promotion research. Williams JBW, Kobak KA. Development and reliability of a structured interview
– Date of approval: April 2016. guide for the Montgomery-Asberg Depression Rating Scale (SIGMA). Br J
Psychiatry. 2008;192(1):52–8.
Competing interests Willison HJ, Jacobs BC, van Doorn PA. Guillain-Barré syndrome. Lancet. 2016;
The authors declare that they have no competing interests. 388:717–27.

Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in
published maps and institutional affiliations.

Author details
1
Department of Neuropsychiatry, Faculty of Medicine, Tanta University, Tanta
31527, Egypt. 2Psychiatry Unit, Department of Neuropsychiatry, Faculty of
Medicine, Tanta University, Tanta, Egypt. 3Chest Diseases Department, Faculty
of Medicine, Tanta University, Tanta, Egypt.

Received: 4 October 2017 Accepted: 23 March 2018

References
Alshekhlee A, Hussain Z, Sultan B, Katirji B. Guillain-Barré syndrome: incidence and
mortality rates in US hospitals. Neurology. 2008;70:1608–13.
Bernsen RA, De JagerAE KW, Van Der Meché F, Suurmeijer TP. Psychosocial
dysfunction in the first year after Guillain Barré Syndrome. Muscle Nerve.
2010;41:533–9.
Brousseau K, Arciniegas D, Harris S. Pharmacologic management of anxiety and
affective lability during recovery from Guillain Barré syndrome: some
preliminary observations. Neuropsychiatr Dis Treat. 2005;1(2):145–9.
Chokroverty S. Sleep dysfunction in neuromuscular disorders. Schweiz Arch
Neurol Psychiatr. 2003;154:400–6.
Cochen V, Arnulf I, Demeret S, Neulat ML, Gourlet V, Drouot X, et al. Vivid
dreams, hallucinations, psychosis and REM sleep in Guillain Barré syndrome.
Brain. 2005;128:2535–45.
Darweesh SKL, Polinder S, Mulder MJHL, Baena CP. Health-related quality of life in
Guillain Barré syndrome patients: a systematic review. J Peripher Nerv Syst.
2014;19:24–35.
Fokke C, van den Berg B, Drenthen J, Walgaard C, van Doorn PA, Jacobs BC.
Diagnosis of Guillain-Barré syndrome and validation of Brighton criteria.
Brain. 2014;137:33–43.
Gao J, Li Y, Sun Y, Hu W, Liu Y, An D, Yin Y. The study of sleep disorder factors in
patients with Guillain-Barré syndrome. Int J Neurosci. 2016;126(10):893–8.
https://doi.org/10.3109/00207454.2015.1080699.
González-Suárez I, Sanz-Gallego I, de Rivera FJR, Arpa J. Guillain-Barré syndrome:
natural history and prognostic factors: a retrospective review of 106 cases.
BMC Neurol. 2013;13:95–101.
Goodfellow JA, Wilson HJ. Guillain Barré Syndrome: a century of progress. Nat
Rev Neurol. 2016;12(12):723–31.
Grigg-Damberger MM. The AASM scoring manual four years later. J Clin Sleep
Med. 2012;8(3):323–32. https://doi.org/10.5664/jcsm.1928.
Jensen MP, Friedman M, Bonzo D, Richard P. The validity of neuropathic pain
scale for assessing diabetic neuropathic pain in a clinical trial. Clin J Pain.
2006;22(1):97–103.
Karkare K, Sinha S, Taly AB, Rao S. Prevalence and profile of sleep disturbances in
Guillain-Barre syndrome: a prospective questionnaire based study during 10
days of hospitalization. Acta Neurol Scand. 2013;127:116–23.
Maier W, Buller R, Philipp M, Heuser I. The Hamilton Anxiety Scale: reliability,
validity and sensitivity to change in anxiety and depressive disorders. J Affect
Disord. 1988;14(1):61–8.
Meena AK, Khadilkar SV, Murthy JMK. Treatment guidelines for Guillain–Barré
Syndrome. Ann Indian Acad Neurol. 2011;14:73–81.
Merkies ISJ, Schmitz PIM, van der Meché FGA, Samijn JPA, van Doorn PA.
Clinimetric evaluation of a new overall disability scale in immune mediated
polyneuropathies. J Neurol Neurosurg Psychiatry. 2002;72:596–601.
Peralta A, Bentes C, Santos R. Clinical and polysomnographic status dissociatus in
Guillain Barre syndrome. Clin Neurophysiol. 2006;117:106–7.
van den Berg B, Walgaard C, Drenthen J, Fokke C, Jacobs BC, van Doorn PA.
Guillain–Barré syndrome: pathogenesis, diagnosis, treatment and prognosis.
Nat Rev Neurol. 2014;10(8):469–82.

You might also like