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Original Article

Early clinical and electrophysiologic predictors of a complicated clinical course in Guillain-Barré syndrome: a 14-year retrospective study

Annals of Clinical Neurophysiology 2025;27(2):52-66.
Published online: October 31, 2025

Department of Neurology, Institute of the Neurological Sciences, The Medical City, Metro Manila, Philippines

Correspondence to Marvic Joseph S. Amoranto Department of Neurology, Institute of the Neurological Sciences, The Medical City, Metro Manila 1604, Philippines Tel: +63-933-855-2143 E-mail: mjs.amoranto@gmail.com
• Received: May 29, 2025   • Revised: September 15, 2025   • Accepted: September 30, 2025

© 2025 The Korean Society of Clinical Neurophysiology

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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  • Background
    Electromyography and nerve conduction studies (EMG-NCS) often yield nonspecific findings during the early stage of Guillain-Barré syndrome (GBS). Although useful for diagnosis, EMG-NCS are traditionally of little value in predicting a complicated clinical course, which is critical for timely decisions to initiate immunomodulatory treatment. We aimed to identify the early clinical and electrophysiologic predictors of respiratory failure, a prolonged hospital stay, and moderate-to-severe disability at discharge in GBS.
  • Methods
    We retrospectively analyzed the clinical and electrophysiologic data of adult GBS patients who were hospitalized during the early course of the disease (<2 weeks from symptom onset).
  • Results
    Eighty-one patients aged 47.5 ± 16.1 years were analyzed. The most common clinical variants were Miller-Fisher syndrome (30.9%) and classic sensorimotor GBS (25.9%). The clinical variant was not predictive of a complicated clinical course. Instead, specific clinical features such as dysautonomia (p = 0.006) and marked motor deficits (p = 0.002) were predictive of the primary composite outcome of respiratory failure and/or a prolonged hospital stay, with dysautonomia (p = 0.035) also predictive of moderate-to-severe disability at discharge. The most common abnormalities in EMG-NCS were bilateral absence of the H-reflex (86.4%) and F-wave abnormalities (44.4%). The presence of F-wave abnormalities was predictive of both respiratory failure (p = 0.032) and a prolonged hospital stay (p = 0.001).
  • Conclusions
    Early F-wave abnormalities in GBS may serve as an electrophysiologic predictor of a complicated clinical course, suggesting that EMG-NCS can provide prognostic information to guide treatment decisions during the early stage of the disease.
Guillain-Barré syndrome (GBS) is the leading cause of acute flaccid paralysis worldwide, with a reported incidence ranging from 1.1 to 1.8 cases per 100,000 people per year.1,2 It is an acute inflammatory disorder of the peripheral nervous system that typically presents with symmetrical sensorimotor symptoms that often begin in the lower extremities and progress in diverse clinical patterns.3-6 GBS is primarily diagnosed clinically with the aid of electromyography and nerve conduction studies (EMG-NCS).2,4-6 However, during the early stage of the disease, EMG-NCS often yield nonspecific findings that serve mainly to support the diagnosis and exclude mimics, while offering little utility in guiding treatment decisions.7
In the Philippines, clinical practices for GBS largely adhere to international guidelines, which recommend initiating intravenous immunoglobulin (IVIg) or plasma exchange (PLEX) in patients with severe features such as nonambulation, bulbar dysfunction, dysautonomia, and respiratory insufficiency.2,4,7,8 In contrast, stable ambulatory patients are usually observed and managed supportively.3 However, predicting which patients will ultimately require immunomodulatory treatment remains difficult, particularly during the early uncomplicated stage of the disease. This is a critical concern in the Philippine setting where treatment costs frequently result in delays that conflict with the efficacy window of IVIg and PLEX being confined to the first 2 weeks and 4 weeks after symptom onset, respectively.2,4 The costs at one of the largest government tertiary referral centers in the country far exceed the average monthly Filipino household income, which prevents many patients from receiving treatment.3,9 Treatment costs are even higher in private institutions such as ours-The Medical City, the flagship complex of the largest healthcare network in the country10-since medication prices in such institutions are not subject to government-imposed ceilings.9 Our experience at this institution is that treatment delays are encountered despite the onset of definitive clinical indications due to some patients needing to reallocate personal resources, liquidate assets, or rely on government assistance, which increases the risk of missing the therapeutic window. This interplay of time-restricted efficacy and financial burden complicates treatment decisions due to them frequently needing to be made earlier to account for the anticipated delays.
The ability to identify early clinical features predictive of the subsequent need for treatment would be advantageous to both patients and clinicians by facilitating its preparation and procurement earlier during the disease course, rather than deferring interventions until definitive clinical indications arise. Given that current guidelines rely heavily on clinical parameters, we hypothesized that evaluating the association of electrophysiologic features with a complicated clinical course, such as respiratory failure and prolonged hospitalization, will extend the role of EMG-NCS beyond diagnostic support to informing early treatment decisions. To test this hypothesis, this study aimed to describe the clinical and electrophysiologic features of GBS patients within the first 2 weeks after symptom onset, and identify the early clinical and nonspecific EMG-NCS findings that could be utilized as predictors of the development of respiratory failure, a prolonged hospital stay, and moderate-to-severe disability at discharge.
Research design and setting
This retrospective cohort study involved adult patients diagnosed with GBS in The Medical City, a tertiary hospital in metropolitan Manila, the Philippines. Medical records of patients who were hospitalized from January 2010 to March 2024 were included in the chart review process. This study was approved by the Institutional Review Board with registry number GCS NS 2-24-026, in accordance with the guidelines of the International Conference on Harmonization of Good Clinical Practice and Data Privacy Act of 2012.
Data collection instruments
Patients with GBS were identified in the electronic database of the medical records department of The Medical City. The search strategy employed the 10th revision of the International Classification of Diseases codes for identifying primary and secondary diagnoses of GBS. The chart review process utilized the medical information documentation and access system and the hospital information system. EMG-NCS reports were retrieved from the neurophysiology laboratory of The Medical City. Clinical data were organized in an encrypted Microsoft Excel 2021 file (Microsoft Corporation, Redmond, WA, USA), with random numbers used as patient identifiers.
Patient selection
The following inclusion criteria were applied for patient selection: adults aged 19 years and above; having a premorbid Katz index of independence in activities of daily living (Katz ADL score) of 5 or 6, indicating full functional capacity prior to the illness; having a final diagnosis of GBS as assessed by a neurologist, including all levels of diagnostic certainty in the Brighton criteria;6 and having both EMG and NCS performed and interpreted by an electromyographer within <14 days from the onset of symptoms. Patients who were transferred to another hospital or opted to be discharged against medical advice as well as those with other known causes of polyneuropathy or other conditions in their past medical history that may confound the EMG-NCS findings (e.g., diabetic polyneuropathy, toxic-metabolic polyneuropathy, demyelinating diseases, or neuromuscular disease) or with clinical conditions with a high predisposition to an underlying polyneuropathy (e.g., uncontrolled diabetes mellitus [DM], previous treatment with platinum-based agents, taxanes, or vinca alkaloids) were excluded. Patients who had DM were included if all of the following were fulfilled: diagnosed with DM within the previous 1 year, no history of symptoms suggestive of an underlying polyneuropathy (e.g., paresthesia, numbness, or neuropathic pain) or poor sugar control (e.g., polyuria, polydipsia, or polyphagia) prior to the onset of GBS, a glycated hemoglobin level of <7.0% within the previous 3 months, and a random blood sugar level of <200 mg/dL upon hospitalization. Patients who were intubated prior to EMG-NCS, who were admitted for another critical condition but eventually developed GBS during the hospital stay, or whose clinical records were incomplete for the medical history and neurologic examination were also excluded.
Data sets
Data on demographics, clinical manifestations, electrophysiologic features, and outcome were obtained utilizing a case report form (Supplementary Table 1).
Demographic data and history
Demographic and historical data such as age, sex, seasonal occurrence, presence of comorbidities, vaccination history, antecedent infection, time to the onset of symptoms from antecedent infection, and duration of GBS symptoms upon hospitalization were obtained.
Clinical manifestations
The assessed clinical parameters comprised marked motor deficits, sensory deficits, cranial nerve deficits, signs of dysautonomia, and the clinical variant2 (Supplementary Table 2), all of which were obtained when EMG-NCS were performed. Marked motor deficits were defined by the presence of any of the following: a medical research council score of ≤2 (out of 5) for the upper or lower extremities, neck weakness, or ataxia. Sensory deficits comprised the presence of paresthesia, numbness, or radicular pain, while cranial nerve deficits comprised the presence of bulbar palsy, ocular palsy, or facial diplegia. Signs of dysautonomia were operationally modified based on the criteria applied by Bazán-Rodríguez et al.11 and Tewedaj et al.12 as listed in Supplementary Table 3, and only signs of dysautonomia that had occurred prior to performing EMG-NCS were included. The level of diagnostic certainty based on the Brighton criteria,6 presence of albuminocytologic dissociation in the cerebrospinal fluid, and immunomodulatory treatment given (IVIg or PLEX) were also obtained.
Electrophysiologic features
The nonspecific NCS parameters included abnormalities in the compound muscle action potential (CMAP) and sensory nerve action potential (SNAP), comprising prolonged distal latencies, decreased distal amplitudes, slowing of conduction velocities (CVs), and presence of conduction block and unexcitable nerves. Conduction block was defined according to Hadden et al.13 as a proximal-to-distal CMAP amplitude ratio of <0.5, with a distal CMAP amplitude of ≥20% of the lower limit of normal. The CMAP and SNAP abnormalities were assessed only in nerves that are routinely included in NCS: ulnar, peroneal, and tibial nerves for CMAPs; ulnar, sural, and superficial peroneal nerves for SNAPs. For the late responses, bilateral absence of the H-reflex and F-wave abnormalities (prolonged latency or absence) in any upper or lower extremity nerve were included. CMAP, SNAP, and F-wave abnormalities of the median nerve were disregarded since this is an entrapment site,14 and findings obtained for additional nerves not included in routine NCS testing (e.g., radial nerve) were excluded. Reference values were based from the institutional standard employed by the neurophysiology laboratory of The Medical City. The primary pathology was determined as axonal, demyelinating, or equivocal according to the criteria of Hadden et al.13
The nonspecific EMG parameters comprised the presence of abnormal spontaneous activities (increased insertional activity, positive sharp waves, fibrillations, or fasciculations) and abnormal volitional motor unit action potentials (reduced recruitment, polyphasic potentials, increased duration, increased amplitude, or abnormal configuration).
Outcome measures
The primary outcome was a complicated clinical course, which was operationally defined as the occurrence of respiratory failure requiring mechanical ventilation (MV), a prolonged hospital stay (≥15 days), or both. This composite outcome was chosen to encompass clinically significant morbidities, recognizing that respiratory failure and prolonged hospitalization represent overlapping but not mutually exclusive indicators of disease severity that are primary targets of GBS treatment. Hospital stay was defined as the duration of active hospitalization from the time of admission until the patient was medically cleared for discharge, excluding additional periods attributable to nonclinical factors such as administrative delays or arrangements for home care. The cutoff for a prolonged hospital stay was derived from the local study of I Espiritu et al.,3 who reported that the median hospital stay was 15 days for GBS patients in one of the largest tertiary referral centers in the Philippines.
The secondary outcome was the degree of disability at discharge as measured by the Guillain-Barré syndrome disability score (GBS-DS), which is a widely accepted scoring system for assessing the functional status of GBS patients.4,7 The scores were dichotomized into minimal disability (scores of 0-3) and moderate-to-severe disability or death (scores of 4-6), effectively categorizing an outcome as ambulatory (irrespective of any need for assistance) or nonambulatory.
Statistical analyses
Descriptive statistics were used to summarize the demographic, clinical, and electrophysiologic features of the patients, with numbers and proportions used for categorical variables, medians and interquartile ranges (IQRs) for non-normally distributed continuous variables, and mean ± standard-deviation values for normally distributed continuous variables. The independent-samples t-test, Mann-Whitney U-test, and Fisher’s exact/chi-square test were used to identify significant differences in the mean, rank, and frequency, respectively, between patients with and without a complicated clinical course. A stepwise selection method was utilized to identify independent variables that did not demonstrate multicollinearity. Variables meeting this criterion were subsequently included in the final multivariate regression model to identify independent predictors of the specified outcome measure. This approach ensured model stability and minimized bias arising from collinearity. Odds ratios (ORs) and their corresponding 95% confidence intervals (CIs) were computed in binary logistic regression analyses to identify significant predictors of respiratory failure, a prolonged hospital stay, and moderate-to-severe disability at discharge.
All statistical tests were performed as two-tailed tests. The Shapiro-Wilk test was used to check whether the continuous variables conformed to a normal distribution. Missing values were neither replaced nor estimated. Null hypotheses were rejected at the α = 0.05 level of significance. Microsoft Excel 2021 and STATA 13.1 (StataCorp LP, College Station, TX, USA) were used for data management and analyses, respectively.
Patient selection
This study retrieved the clinical records of 116 patients with a primary or secondary diagnosis of GBS from January 2010 to March 2024. Applying the eligibility criteria resulted in 35 patients being excluded: 14 pediatric patients, three who did not undergo EMG-NCS, two who underwent EMG-NCS beyond the early stage of the disease (≥14 days), four who did not have GBS as the final diagnosis, nine with uncontrolled DM or symptoms of poor sugar control prior to the illness, two with a Katz ADL score of ≤4 prior to the illness, and one who had undergone recent chemotherapy with paclitaxel. Hence, 81 patients with a diagnosis of GBS with EMG-NCS performed during the early stage of the disease were finally included in the study (Fig. 1).
Demographics and clinical history
Patients with and without a complicated clinical course (i.e., respiratory failure and/or a prolonged hospital stay) were compared as the primary composite outcome (Table 1). The patients were aged 47.5 ± 16.1 years, and there was a moderate female predominance (female-to-male ratio of 1.38:1). Most patients were diagnosed during the rainy (n = 41 [50.6%]) and cool dry (n = 25 [30.9%]) seasons. Hypertension was the most common comorbidity (n = 29 [35.8%]), followed by type 2 DM (n = 12 [14.8%]) and dyslipidemia (n = 9 [11.1%]). Only two patients had recently been vaccinated prior to their illness. Most patients had an antecedent infection (n = 59 [72.8%]), with respiratory infections being the most common (n = 42 [51.9%]). The median delay from the antecedent infection to the onset of GBS symptoms was 7 days (IQR, 4-8 days), and the median interval from the onset of GBS symptoms to hospitalization was 4 days (IQR, 2-6 days). There were no significant differences in demographics or baseline clinical history between those with and without a complicated clinical course, except for an antecedent gastrointestinal infection being more common among those in the former group (p = 0.022).
Clinical manifestations
There was a wide distribution in the clinical variant of GBS, with Miller-Fisher syndrome (n = 25 [30.9%]) and classic sensorimotor GBS (n = 21 [25.9%]) being the most common, but it did not differ significantly between the two groups. However, considering the clinical manifestations individually revealed that the following were more common in those with a complicated clinical course: presence of marked motor deficits (p = 0.004) with diplegia of upper extremities (p = 0.002) and lower extremities (p < 0.001) and neck flexor weakness (p < 0.001), cranial nerve deficits (p = 0.001) with bulbar involvement (p < 0.001), and dysautonomia (p < 0.001) with blood pressure (p < 0.001) and heart rate (p < 0.001) fluctuations (Table 1).
Most of the patients fulfilled level 2 of the Brighton criteria for the diagnosis of GBS (n = 54 [66.7%]), while 5 (6.2%) fulfilled level 1 since only 12 patients in this cohort underwent lumbar puncture. Lower levels of diagnostic certainty (Brighton criteria level of 3 or 4) (p = 0.022) were more common in patients who did not have a complicated clinical course, likely reflecting the milder manifestations in these levels. Immunomodulatory treatment with IVIg or PLEX was administered more frequently to patients who eventually had a complicated clinical course (p = 0.002).
EMG and NCS
The illness duration when EMG-NCS were performed was 5.7 ± 2.9 days, with no significant difference between the two groups (Table 2). Patients with a complicated clinical course were significantly more likely to exhibit the presence of decreased distal CMAP amplitudes (p = 0.002), particularly of the ulnar nerve (p = 0.010), unexcitable CMAPs of the ulnar (p = 0.008) and tibial (p = 0.005) nerves, and unexcitable SNAPs (p = 0.009), particularly of the sural nerve (p = 0.021). Bilateral absence of the H-reflex was the most common NCS abnormality in this cohort, being observed in 70 (86.4%) patients, but the occurrence of this finding did not significantly differ between patients with and without a complicated clinical course. In contrast, prolonged or absent F-waves were present in 36 (44.4%) patients, and these abnormalities were significantly more common in patients with a complicated clinical course (p < 0.001). The primary pathology did not differ between the two groups; however, a demonstrable pathology (demyelinating or axonal) was significantly more common in patients with a complicated clinical course (p = 0.006). EMG findings showed that abnormal spontaneous activity (p = 0.47), particularly increased insertional activity (p = 0.023) and the presence of fibrillations (p = 0.026), was significantly more common in patients with a complicated clinical course. Repeat EMG-NCS were performed in 11 patients in this cohort; they had a median duration of illness of 22 days (IQR, 16-60 days) and 9 of them already demonstrated a specific subtype of GBS, while the other 2 remained equivocal.
Clinical course
A complicated clinical course was observed in 32 (39.5%) patients, comprising 13 (16.1%) with a prolonged hospital stay alone, 1 (1.2%) with isolated respiratory failure, and 18 (22.2%) with both outcomes. Overall, the hospital stay was prolonged in 31 (38.3%) patients and respiratory failure occurred in 19 (23.5%) patients, with a median duration of MV dependence of 10 days (IQR, 8-14 days). All but one of the patients who developed respiratory failure also had a prolonged hospital stay. In contrast, 49 (60.5%) patients did not experience any of these outcomes (Table 3).
Factors associated with a complicated clinical course
After adjusting for other variables, the clinical and electrophysiologic predictors of a complicated clinical course were the presence of marked motor deficits (OR, 10.21; 95% CI, 2.31-45.2; p = 0.002), dysautonomia (OR, 14.42; 95% CI, 2.16-96.1; p = 0.006), and F-wave abnormalities (OR, 8.00; 95% CI, 2.29-27.9; p = 0.001). Analyzing the individual components of the primary composite outcome revealed the same factors as predictors of a prolonged hospital stay alone, whereas dysautonomia (p < 0.001) and F-wave abnormalities (p = 0.032) remained predictors of the development of respiratory failure alone (Table 4). The retention of essentially the same factors was probably due to the high frequency of a prolonged hospital stay among patients with respiratory failure.
Factors associated with moderate-to-severe disability at discharge
The clinical features that appeared to be associated with moderate-to-severe disability at discharge in the univariate analyses were age, dysautonomia, decreased distal CMAP amplitude, F-wave abnormalities, axonal pathology, and the presence of abnormal spontaneous activities. After adjusting for other variables, higher age (OR, 1.07; 95% CI, 1.02-1.12; p = 0.006), dysautonomia (OR, 5.00; 95% CI, 1.12-22.4; p = 0.035) and axonal pathology (OR, 17.52; 95% CI, 1.31-234.0; p = 0.030) were the predictors of moderate-to-severe disability at discharge.
We have identified clinical and electrophysiologic predictors of respiratory failure, a prolonged hospital stay, and moderate-to-severe disability at discharge in GBS within the first 2 weeks after symptom onset. The identified factors represent potential early indicators for guiding timely treatment decisions in GBS.
Among clinical manifestations, the clinical variant of GBS during the early stage of the disease was not predictive of a complicated clinical course or moderate-to-severe disability at discharge; instead, the specific features of marked motor deficits, neck flexor weakness, and dysautonomia were prognostically relevant. Previous studies have consistently found low motor power, bulbar palsy, and neck flexion weakness to be associated with respiratory failure,15-21 most likely reflecting the risk of aspiration pneumonia from bulbar dysfunction and the close anatomical relationship between the neck and respiratory muscle innervation.17 Dysautonomia consistently predicted all outcomes in our cohort and has previously been widely found to be correlated with higher rates of MV, worse functional recovery, and mortality, since it signifies greater involvement of the peripheral nervous system.15,18-20,22,23
The consistent association of these clinical predictors across diverse patient populations-including in our cohort-demonstrates the robustness of their role as key indicators for initiating treatment in clinical practice.2,4,7 In contrast, EMG-NCS have traditionally been regarded as primarily of diagnostic value, with little utility in guiding treatment decisions.7 The inclusion in our analyses of early nonspecific electrophysiologic features has identified the presence of F-wave abnormalities as an independent predictor of both respiratory failure and a prolonged hospital stay, which represents a novel finding of this study. This association has been similarly described in only one adult cohort by Chen et al.24 and in pediatric populations by Lee et al.25 and Prakash et al.,26 all linking F-wave abnormalities to delayed recovery and poor prognosis. These sparse but consistent findings across age groups suggest that F-wave abnormalities represent a clinically relevant prognostic marker that warrants validation in larger prospective studies, which might expand the role of EMG-NCS from a purely diagnostic tool to a determinant for early intervention. In our cohort, EMG-NCS were performed at 5.7 ± 2.9 days from the onset of GBS symptoms, suggesting that F-wave abnormalities detected within the first week of illness can already inform treatment decisions, even before conventional clinical indicators become evident.
F-wave abnormalities reflect proximal demyelination of the nerves,5,24 and their early detection may indicate a more rapid demyelination and disease progression. This may be an electrophysiologic representation of a shorter interval between disease onset and hospital admission, which has previously been established as an early predictor of respiratory failure.24 However, caution is warranted in applying this finding as a predictor of GBS-related outcomes, since F-wave abnormalities also occur in toxic-metabolic polyneuropathies, radiculopathies, and entrapment neuropathies.25 Thus, clinical correlation with the exclusion of other concomitant neuropathies that may confound electrodiagnostic findings is essential before this parameter can be reliably applied as a predictor of GBS-related outcomes. Due to the high susceptibility of the median nerve to entrapment,14 electrophysiologic data from that nerve were excluded from the present analysis, and patients with coexisting neuropathies were likewise excluded from the present study to ensure that the electrophysiologic features reflected changes attributable only to GBS. Hence, F-wave abnormalities could be a useful predictor of GBS-related outcomes only in the proper clinical context, when confounding neuropathies are absent and when the abnormalities are not confined to a known entrapment site.
A primarily axonal pathology in the initial EMG-NCS was also associated with moderate-to-severe disability at discharge. However, it is important to recognize that accurately determining the pathophysiologic process in GBS often requires serial electrodiagnostic studies, since early demyelinating features may later evolve to reveal an underlying axonal pathology.27-29 The primary pathology found in the present study reflects only the apparent pathophysiologic process (or may be equivocal) at a single time point and hence should be applied only within that context. Therefore, nonspecific electrophysiologic parameters such as F-wave abnormalities may be more useful as predictors during the early stage of the disease when the GBS subtype and primary pathology remain uncertain.
Bilateral absence of the H-reflex was the most common early electrophysiologic finding in this cohort, which is consistent with the profiling studies of Rasera et al.5 and Gordon and Wilbourn.30 However, its utility appears restricted to diagnostic sensitivity. It is important to note that only the bilateral absence of the H-reflex is compatible with GBS, whereas the unilateral absence of this reflex is more suggestive of lumbosacral radiculopathy.5 This is why only the bilateral absence of this reflex was considered as the pertinent H-reflex abnormality in the present study. While this finding reliably supports the early diagnosis of GBS in the proper clinical context, it did not distinguish between patients with and without a complicated clinical course. Thus, unlike F-wave abnormalities, its clinical relevance appears primarily restricted to supporting the diagnosis rather than informing the prognosis.
F-wave abnormalities and axonal pathology were the only electrophysiologic features found to be independently associated with our outcomes after adjusting for other variables. In a similar study, Durand et al.29 found that a common peroneal nerve proximal-to-distal CMAP amplitude ratio of >0.556 was associated with a lower risk of requiring MV. This specific association was not reproduced in our cohort, probably due to methodologic differences: Durand et al.29 also analyzed the CMAP amplitude ratio as a continuous variable to identify an optimal threshold, whereas our study applied only the dichotomized definition of conduction block (with a cutoff of 0.5) as conventionally obtained in standard protocols for EMG-NCS. This limitation of our study may have obscured subtle gradations in the CMAP amplitude ratio that could be clinically relevant but did not meet the conventional criteria for the presence of a conduction block.
Other limitations of the study include the exclusion of laboratory parameters such as complete blood count, liver enzymes, and electrolytes as potential early predictors of the observed outcomes. Also, the GBS-DS at discharge might not be the most reliable measure of disability outcome, since the recovery from GBS might not peak until weeks or even months after discharge. In addition, the retrospective nature of data collection meant that there was an inherent risk of recording bias and unaccounted confounding factors. Our attempts to mitigate these issues included applying stringent inclusion and exclusion criteria to minimize the impact of unrecognized confounders. We recommend that electrophysiologic predictors be applied only to guide early treatment decisions in patients who have not yet fulfilled the established clinical indications for intervention during the early stage of the disease, particularly in circumstances where treatment delays are anticipated. Moreover, prospective studies are warranted to further validate the present findings, including postdischarge observations that provide adequate follow-up assessments of patient recovery and disability outcomes. Nonetheless, the comprehensive analyses performed in the present study have identified associations between electrophysiologic parameters and clinical outcomes that support the formulation of promising hypotheses for testing in larger prospective investigations.
We conclude that the present findings reaffirm the predictive value of dysautonomia and marked motor deficits for a complicated clinical course in GBS, with dysautonomia also being predictive of moderate-to-severe disability at discharge. Beyond these established associations, the presence of F-wave abnormalities was found to be an independent predictor of both respiratory failure and a prolonged hospital stay, highlighting the potential of early EMG-NCS to provide prognostic information beyond its conventional diagnostic role, which is crucial in settings where treatment delays are common. Larger prospective studies are needed to further validate whether F-wave abnormalities are a reliable electrophysiologic marker for guiding timely treatment decisions during the early stage of GBS.

Supplementary Table 1.

Case report form
acn-25006-Supplementary-Table-1.pdf

Supplementary Table 2.

Clinical variant
acn-25006-Supplementary-Table-2.pdf

Supplementary Table 3.

Criteria for dysautonomia
acn-25006-Supplementary-Table-3.pdf

Conflicts of Interest

The authors have no potential conflicts of interest to disclose.

Funding

None.

Acknowledgements

We extend our sincere gratitude to Dr. Nika Reyes and Dr. Maria Angela Pura for their intellectual contributions to this study. We also thank Mr. Armel Mendoza for his unwavering assistance throughout the course of this work.

Fig. 1.
Patient selection process. GBS, Guillain-Barré syndrome; DM, diabetes mellitus.
acn-25006f1.jpg
Table 1.
Demographic and clinical features of the patients
Total (n = 81) Respiratory failure and/or prolonged hospital stay
p-value
With (n = 32) Without (n = 49)
Demographics
 Age (years) 47.5 ± 16.1 51.5 ± 18.1 44.8 ± 14.3 0.066
 Sex 1.000
  Male 34 (42.0) 13 (40.6) 21 (42.9)
  Female 47 (58.0) 19 (59.4) 28 (57.1)
 Season 0.625
  Rainy 41 (50.6) 14 (43.8) 27 (55.1)
  Cool dry 25 (30.9) 11 (34.4) 14 (28.6)
  Hot dry 15 (18.5) 7 (21.9) 8 (16.3)
History
 Comorbiditiesa
  Hypertension 29 (35.8) 13 (40.6) 16 (32.7) 0.486
  Diabetes mellitus 12 (14.8) 3 (9.4) 9 (18.4) 0.347
  Dyslipidemia 9 (11.1) 5 (15.6) 4 (8.2) 0.471
  Bronchial asthma 4 (4.9) 2 (6.3) 2 (4.1) 0.646
  Others 19 (23.5) 8 (25.0) 11 (22.4) 0.795
 Recent vaccination 2 (2.5) 1 (3.1) 1 (2.0) 1.000
 Antecedent infectiona 59 (72.8) 25 (78.1) 34 (69.4) 0.451
  URTI 42 (51.9) 14 (43.8) 28 (57.1) 0.263
  GI 15 (18.5) 10 (31.3) 5 (10.2) 0.022b
  UTI 3 (3.7) 1 (3.1) 2 (4.1) 1.000
  Cutaneous 1 (1.2) 1 (3.1) 0 (0.0) 0.395
 Onset of GBS symptoms from antecedent infection (days) 7 (4 to 8) 7 (6 to 11) 7 (4 to 7) 0.107
 Duration of GBS symptoms upon hospitalization (days) 4 (2 to 6) 5 (2.5 to 6) 4 (2 to 6) 0.251
Clinical manifestations
 Clinical variant
  MFS 25 (30.9) 7 (21.9) 18 (36.7) 0.219
  Classic sensorimotor GBS 21 (25.9) 11 (34.4) 10 (20.4) 0.198
  Pure motor 13 (16.0) 6 (18.8) 7 (14.3) 0.758
  MFS-GBS overlap 8 (9.9) 4 (12.5) 4 (8.2) 0.706
  Bilateral facial palsy with paraesthesias 5 (6.2) 2 (6.3) 3 (6.1) 1.000
  Pharyngeal-cervical-brachial 4 (4.9) 2 (6.3) 2 (4.1) 0.646
  Pure sensory 3 (3.7) 0 (0.0) 3 (6.1) 0.274
  Paraparetic 2 (2.5) 0 (0.0) 2 (4.1) 0.516
 Marked motor deficitsa 53 (65.4) 27 (84.4) 26 (53.1) 0.004b
  Diplegia of upper extremities 18 (22.2) 13 (40.6) 5 (10.2) 0.002b
  Diplegia of lower extremities 21 (25.9) 17 (53.1) 4 (8.2) <0.001b
  Neck flexor weakness 23 (28.4) 18 (56.3) 5 (10.2) <0.001b
  Ataxia 26 (32.1) 7 (21.9) 19 (38.8) 0.146
 Sensory deficitsa 51 (63.0) 21 (65.6) 30 (61.2) 0.815
  Paresthesia 47 (58.0) 19 (59.4) 28 (57.1) 1.000
  Numbness 37 (45.7) 17 (53.1) 20 (40.8) 0.362
  Radicular pain 2 (2.5) 1 (3.1) 1 (2.0) 1.000
 Cranial nerve deficitsa 63 (77.8) 31 (96.9) 32 (65.3) 0.001b
  Bulbar 45 (55.6) 27 (84.4) 18 (36.7) <0.001b
  Ocular 36 (44.4) 14 (43.8) 22 (44.9) 1.000
  Facial diplegia 16 (19.8) 8 (25.0) 8 (16.3) 0.398
 Dysautonomiaa 17 (21.0) 14 (43.8) 3 (6.1) <0.001b
  BP fluctuations 17 (21.0) 14 (43.8) 3 (6.1) <0.001b
  HR fluctuations 13 (16.0) 12 (37.5) 1 (2.0) <0.001b
  Gastrointestinal dysfunction 2 (2.5) 2 (6.3) 0 (0.0) 0.153
  Sudomotor dysfunction 1 (1.2) 1 (3.1) 0 (0.0) 0.395
  Genitourinary dysfunction 0 (0.0) 0 (0.0) 0 (0.0)
Cerebrospinal fluid
 Albuminocytologic dissociation 0.494
  Yes 11 (13.6) 5 (15.6) 6 (12.2)
  No 1 (1.2) 1 (3.1) 0 (0.0)
  CSF not obtained 69 (85.2) 26 (81.3) 43 (87.8)
Diagnostic certainty
 Brighton criteria 0.022b
  1 5 (6.2) 3 (9.4) 2 (4.1)
  2 54 (66.7) 26 (81.3) 28 (57.1)
  3 10 (12.3) 2 (6.3) 8 (16.3)
  4 12 (14.8) 1 (3.1) 11 (22.4)
Intervention
 Treatment given 0.002b
  None 13 (16.0) 0 (0.0) 13 (26.5)
  IVIg 57 (70.4) 27 (84.4) 30 (61.2)
  PLEX 11 (13.6) 5 (15.6) 6 (12.2)

Values are presented as mean ± standard deviation, number (%), median (interquartile range). Mutually exclusive categories may not sum up to 100% because of rounding.

URTI, upper respiratory tract infection; GI, gastrointestinal infections; UTI, urinary tract infection; GBS, Guillain-Barré syndrome; MFS, Miller-Fisher syndrome; MFS-GBS, Miller-Fisher syndrome and Guillain-Barre syndrome overlap; BP, blood pressure; HR, heart rate; CSF, cerebrospinal fluid; IVIg, intravenous immunoglobulin; PLEX, plasma exchange.

aPercentages may not sum up to the total because categories are not mutually exclusive.

bp < 0.05.

Table 2.
Findings from electromyography and nerve conduction studies of the patients
Total (n = 81) Respiratory failure and/or prolonged hospital stay
p-value
With (n = 32) Without (n = 49)
Timing of EMG-NCS
 Day of illness EMG-NCS was performed (days) 5.7 ± 2.9 6.0 ± 2.8 5.5 ± 2.9 0.442
CMAP
 Prolonged distal latencya 17 (21.0) 8 (25.0) 9 (18.4) 0.579
  Ulnar 10 (12.3) 5 (15.6) 5 (10.2) 0.505
  Peroneal 13 (16.0) 5 (15.6) 8 (16.3) 1.000
  Tibial 6 (7.4) 2 (6.3) 4 (8.2) 1.000
 CV slowinga 14 (17.3) 8 (25.0) 6 (12.2) 0.228
  Ulnar 10 (12.3) 6 (18.8) 4 (8.2) 0.182
  Peroneal 10 (12.3) 4 (12.5) 6 (12.2) 1.000
  Tibial 2 (2.5) 1 (3.1) 1 (2.0) 1.000
 Conduction blocka 8 (9.9) 3 (9.4) 5 (10.2) 1.000
  Ulnar 4 (4.9) 2 (6.3) 2 (4.1) 0.646
  Peroneal 8 (9.9) 3 (9.4) 5 (10.2) 1.000
  Tibial 2 (2.5) 2 (6.3) 0 (0.0) 0.153
 Decreased distal amplitudea 22 (27.2) 15 (46.9) 7 (14.3) 0.002b
  Ulnar 12 (14.8) 9 (28.1) 3 (6.1) 0.010b
  Peroneal 11 (13.6) 6 (18.8) 5 (10.2) 0.328
  Tibial 12 (14.8) 7 (21.9) 5 (10.2) 0.203
 Unexcitable nervesa 14 (17.3) 8 (25.0) 6 (12.2) 0.228
  Ulnar 5 (6.2) 5 (15.6) 0 (0.0) 0.008b
  Peroneal 12 (14.8) 7 (21.9) 5 (10.2) 0.102
  Tibial 8 (9.9) 7 (21.9) 1 (2.0) 0.005b
SNAP
 Prolonged distal latencya 4 (4.9) 2 (6.3) 2 (4.1) 0.646
  Ulnar 3 (3.7) 2 (6.3) 1 (2.0) 0.559
  Sural 3 (3.7) 1 (3.1) 2 (4.1) 1.000
  Superficial peroneal 2 (2.5) 1 (3.1) 1 (2.0) 1.000
 CV slowinga 3 (3.7) 3 (9.4) 0 (0.0) 0.058
  Ulnar 2 (2.5) 2 (6.3) 0 (0.0) 0.153
  Sural 1 (1.2) 1 (3.1) 0 (0.0) 0.395
  Superficial peroneal 1 (1.2) 1 (3.1) 0 (0.0) 0.395
 Decreased distal amplitudea 6 (7.4) 1 (3.1) 5 (10.2) 0.395
  Ulnar 4 (4.9) 0 (0.0) 4 (8.2) 0.149
  Sural 1 (1.2) 1 (3.1) 0 (0.0) 0.395
  Superficial peroneal 1 (1.2) 0 (0.0) 1 (2.0) 1.000
 Unexcitable nervesa 20 (24.7) 13 (40.6) 7 (14.3) 0.009b
  Ulnar 12 (14.8) 6 (18.8) 6 (12.2) 0.526
  Sural 11 (13.6) 8 (25.0) 3 (6.1) 0.021b
  Superficial peroneal 9 (11.1) 6 (18.8) 3 (6.1) 0.144
Late responses
 H-reflex 0.513
  Normal 11 (13.6) 3 (9.4) 8 (16.3)
  Bilaterally absent 70 (86.4) 29 (90.6) 41 (83.7)
 F-waves <0.001b
  Normal 45 (55.6) 9 (28.1) 36 (73.5)
  Prolonged/absent 36 (44.4) 23 (71.9) 13 (26.5)
Pathophysiologic process
 Primary pathology 0.006b
  Equivocal 36 (44.4) 8 (25.0) 28 (57.1)
  Axonal or demyelinating 45 (55.6) 24 (75.0) 21 (42.9)
Electromyography
 Abnormal spontaneous activitya 16 (19.8) 10 (31.3) 6 (12.2) 0.047b
  Increased insertional activity 11 (13.6) 8 (25.0) 3 (6.1) 0.023b
  PSW 11 (13.6) 7 (21.9) 4 (8.2) 0.105
  Fibrillations 9 (11.1) 7 (21.9) 2 (4.1) 0.026b
  Fasciculations 1 (1.2) 0 (0.0) 1 (2.0) 1.000
 Abnormal volitional MUAPsa 42 (51.9) 20 (62.5) 22 (44.9) 0.174
  Reduced recruitment 42 (51.9) 20 (62.5) 22 (44.9) 0.174
  Polyphasic MUAPs 1 (1.2) 0 (0.0) 1 (2.0) 1.000
  Increased duration 0 (0.0) 0 (0.0) 0 (0.0)
  Increased amplitude 0 (0.0) 0 (0.0) 0 (0.0)
  Abnormal configuration 0 (0.0) 0 (0.0) 0 (0.0)

Values are presented as mean±standard deviation or number (%). Mutually exclusive categories may not sum up to 100% because of rounding.

EMG-NCS, electromyography and nerve conduction studies; CMAP, compound muscle action potential; CV, conduction velocity; SNAP, sensory nerve action potential; PSW, positive sharp waves; MUAP, motor unit action potential.

aPercentages may not sum up to the total because categories are not mutually exclusive.

bp < 0.05.

Table 3.
Prevalence of a complicated clinical course in the study cohort (n = 81)
Complicated clinical course Total cohorta
Any of the following complicated clinical course outcomes (respiratory failure and/or prolonged hospital stay)b 32 (39.5)
 Prolonged hospital stay only (≥15 days) 13 (16.1)
 Respiratory failure only (need for MV) 1 (1.2)
 Both respiratory failure and prolonged hospital stay 18 (22.2)
Prolonged hospital stay (≥15 days)c 31 (38.3)
Respiratory failure (need for MV)d 19 (23.5)
 Length of MV dependence among patients with respiratory failure (days) 10 (8 to 14)
Without any of the complicated clinical course outcomes 49 (60.5)

Values are presented as number (%) or median (interquartile range).

MV, mechanical ventilation.

aPercentages do not sum up to 100% because categories are not mutually exclusive.

bPrimary composite outcome

cWith or without respiratory failure.

dWith or without prolonged hospital stay.

Table 4.
Factors associated with a complicated clinical course and moderate-to-severe disability at discharge
Parameter Univariate
p-value Multivariate
p-value
Crude odds ratio (95% CI) Adjusted odds ratio (95% CI)
Complicated clinical coursea (respiratory failure and/or prolonged hospital stay)
 Antecedent infection
  GI 4.00 (1.22 to 13.1) 0.022
 Clinical manifestations
  Marked motor deficits 4.78 (1.58 to 14.4) 0.006 10.21 (2.31 to 45.2) 0.002
  Cranial nerve deficits 16.47 (2.06 to 131.0) 0.008
  Dysautonomia 11.93 (3.06 to 46.5) <0.001 14.42 (2.16 to 96.1) 0.006
 CMAP
  Decreased distal amplitude 5.29 (1.84 to 15.3) 0.002
 SNAP
  Unexcitable nerves 4.11 (1.41 to 11.9) 0.009
 Late responses
  Prolonged/absent F-waves 7.08 (2.61 to 19.2) <0.001 8.00 (2.29 to 27.9) 0.001
 Primary pathology
  Demyelinating 3.50 (1.14 to 10.7) 0.029
  Axonal 4.67 (1.45 to 15.0) 0.010
 Abnormal spontaneous activity
  Increased insertional activity 5.00 (1.21 to 20.6) 0.026
  Fibrillations 6.44 (1.24 to 33.4) 0.026
Respiratory failurea
 Clinical variant
  Classic sensorimotor GBS 3.75 (1.25 to 11.26) 0.018
 Clinical manifestations
  Dysautonomia 19.54 (5.30 to 72.1) <0.001 13.24 (3.17 to 55.4) <0.001
 CMAP
  Decreased distal amplitude 4.63 (1.54 to 13.9) 0.006
 Late responses
  Prolonged/absent F-waves 7.32 (2.16 to 24.8) 0.001 4.50 (1.14 to 17.8) 0.032
 Abnormal spontaneous activity
  Fibrillations 5.09 (1.21 to 21.4) 0.027
Prolonged hospital staya
 Age (years) 1.03 (1.0003 to 1.06) 0.047
 Clinical manifestations
  Marked motor deficits 4.43 (1.46 to 13.4) 0.008 9.77 (2.18 to 43.7) 0.003
  Cranial nerve deficits 15.45 (1.94 to 123.0) 0.010
  Dysautonomia 12.90 (3.30 to 50.5) <0.001 15.33 (2.26 to 104.0) 0.005
 CMAP
  Decreased distal amplitude 5.76 (1.98 to 16.7) 0.001
 SNAP
  Unexcitable nerves 4.44 (1.52 to 12.9) 0.006
 Late responses
  Prolonged/absent F-waves 8.18 (2.94 to 22.8) <0.001 8.98 (2.51 to 32.1) 0.001
 Primary pathology
  Demyelinating 4.14 (1.31 to 13.1) 0.015
  Axonal 5.52 (1.67 to 18.2) 0.005
 Abnormal spontaneous activity
  Increased insertional activity 5.33 (1.29 to 22.0) 0.021
  Fibrillations 6.85 (1.32 to 35.6) 0.022
Moderate-to-severe disability at discharge (GBS-DS 4-6)a
 Demographics
  Age (years) 1.07 (1.03 to 1.12) 0.001 1.07 (1.02 to 1.12) 0.006
 Clinical manifestations
  Dysautonomia 8.59 (2.41 to 30.6) 0.001 5.00 (1.12 to 22.4) 0.035
 CMAP
  Decreased distal amplitude 3.47 (1.05 to 11.4) 0.041
 Late responses
  Prolonged/absent F-waves 6.16 (1.57 to 24.22) 0.009
 Primary pathology
  Axonal 26.25 (3.0 to 229.0) 0.00 17.52 (1.31 to 234.0) 0.030
 Abnormal spontaneous activity
  PSW 5.56 (1.40 to 22.0) 0.015
  Fibrillations 8.61 (1.94 to 38.2) 0.005

CI, confidence interval; GI, gastrointestinal infections; CMAP, compound muscle action potential; SNAP, sensory nerve action potential; GBS, Guillain-Barré syndrome; GBS-DS, Guillain-Barré syndrome disability scale; PSW, positive sharp waves.

aVariables with p > 0.05 were no longer included.

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      Ann Clin Neurophysiol. 2025;27(2):52-66.   Published online October 31, 2025
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      Early clinical and electrophysiologic predictors of a complicated clinical course in Guillain-Barré syndrome: a 14-year retrospective study
      Image
      Fig. 1. Patient selection process. GBS, Guillain-Barré syndrome; DM, diabetes mellitus.
      Early clinical and electrophysiologic predictors of a complicated clinical course in Guillain-Barré syndrome: a 14-year retrospective study
      Total (n = 81) Respiratory failure and/or prolonged hospital stay
      p-value
      With (n = 32) Without (n = 49)
      Demographics
       Age (years) 47.5 ± 16.1 51.5 ± 18.1 44.8 ± 14.3 0.066
       Sex 1.000
        Male 34 (42.0) 13 (40.6) 21 (42.9)
        Female 47 (58.0) 19 (59.4) 28 (57.1)
       Season 0.625
        Rainy 41 (50.6) 14 (43.8) 27 (55.1)
        Cool dry 25 (30.9) 11 (34.4) 14 (28.6)
        Hot dry 15 (18.5) 7 (21.9) 8 (16.3)
      History
       Comorbiditiesa
        Hypertension 29 (35.8) 13 (40.6) 16 (32.7) 0.486
        Diabetes mellitus 12 (14.8) 3 (9.4) 9 (18.4) 0.347
        Dyslipidemia 9 (11.1) 5 (15.6) 4 (8.2) 0.471
        Bronchial asthma 4 (4.9) 2 (6.3) 2 (4.1) 0.646
        Others 19 (23.5) 8 (25.0) 11 (22.4) 0.795
       Recent vaccination 2 (2.5) 1 (3.1) 1 (2.0) 1.000
       Antecedent infectiona 59 (72.8) 25 (78.1) 34 (69.4) 0.451
        URTI 42 (51.9) 14 (43.8) 28 (57.1) 0.263
        GI 15 (18.5) 10 (31.3) 5 (10.2) 0.022b
        UTI 3 (3.7) 1 (3.1) 2 (4.1) 1.000
        Cutaneous 1 (1.2) 1 (3.1) 0 (0.0) 0.395
       Onset of GBS symptoms from antecedent infection (days) 7 (4 to 8) 7 (6 to 11) 7 (4 to 7) 0.107
       Duration of GBS symptoms upon hospitalization (days) 4 (2 to 6) 5 (2.5 to 6) 4 (2 to 6) 0.251
      Clinical manifestations
       Clinical variant
        MFS 25 (30.9) 7 (21.9) 18 (36.7) 0.219
        Classic sensorimotor GBS 21 (25.9) 11 (34.4) 10 (20.4) 0.198
        Pure motor 13 (16.0) 6 (18.8) 7 (14.3) 0.758
        MFS-GBS overlap 8 (9.9) 4 (12.5) 4 (8.2) 0.706
        Bilateral facial palsy with paraesthesias 5 (6.2) 2 (6.3) 3 (6.1) 1.000
        Pharyngeal-cervical-brachial 4 (4.9) 2 (6.3) 2 (4.1) 0.646
        Pure sensory 3 (3.7) 0 (0.0) 3 (6.1) 0.274
        Paraparetic 2 (2.5) 0 (0.0) 2 (4.1) 0.516
       Marked motor deficitsa 53 (65.4) 27 (84.4) 26 (53.1) 0.004b
        Diplegia of upper extremities 18 (22.2) 13 (40.6) 5 (10.2) 0.002b
        Diplegia of lower extremities 21 (25.9) 17 (53.1) 4 (8.2) <0.001b
        Neck flexor weakness 23 (28.4) 18 (56.3) 5 (10.2) <0.001b
        Ataxia 26 (32.1) 7 (21.9) 19 (38.8) 0.146
       Sensory deficitsa 51 (63.0) 21 (65.6) 30 (61.2) 0.815
        Paresthesia 47 (58.0) 19 (59.4) 28 (57.1) 1.000
        Numbness 37 (45.7) 17 (53.1) 20 (40.8) 0.362
        Radicular pain 2 (2.5) 1 (3.1) 1 (2.0) 1.000
       Cranial nerve deficitsa 63 (77.8) 31 (96.9) 32 (65.3) 0.001b
        Bulbar 45 (55.6) 27 (84.4) 18 (36.7) <0.001b
        Ocular 36 (44.4) 14 (43.8) 22 (44.9) 1.000
        Facial diplegia 16 (19.8) 8 (25.0) 8 (16.3) 0.398
       Dysautonomiaa 17 (21.0) 14 (43.8) 3 (6.1) <0.001b
        BP fluctuations 17 (21.0) 14 (43.8) 3 (6.1) <0.001b
        HR fluctuations 13 (16.0) 12 (37.5) 1 (2.0) <0.001b
        Gastrointestinal dysfunction 2 (2.5) 2 (6.3) 0 (0.0) 0.153
        Sudomotor dysfunction 1 (1.2) 1 (3.1) 0 (0.0) 0.395
        Genitourinary dysfunction 0 (0.0) 0 (0.0) 0 (0.0)
      Cerebrospinal fluid
       Albuminocytologic dissociation 0.494
        Yes 11 (13.6) 5 (15.6) 6 (12.2)
        No 1 (1.2) 1 (3.1) 0 (0.0)
        CSF not obtained 69 (85.2) 26 (81.3) 43 (87.8)
      Diagnostic certainty
       Brighton criteria 0.022b
        1 5 (6.2) 3 (9.4) 2 (4.1)
        2 54 (66.7) 26 (81.3) 28 (57.1)
        3 10 (12.3) 2 (6.3) 8 (16.3)
        4 12 (14.8) 1 (3.1) 11 (22.4)
      Intervention
       Treatment given 0.002b
        None 13 (16.0) 0 (0.0) 13 (26.5)
        IVIg 57 (70.4) 27 (84.4) 30 (61.2)
        PLEX 11 (13.6) 5 (15.6) 6 (12.2)
      Total (n = 81) Respiratory failure and/or prolonged hospital stay
      p-value
      With (n = 32) Without (n = 49)
      Timing of EMG-NCS
       Day of illness EMG-NCS was performed (days) 5.7 ± 2.9 6.0 ± 2.8 5.5 ± 2.9 0.442
      CMAP
       Prolonged distal latencya 17 (21.0) 8 (25.0) 9 (18.4) 0.579
        Ulnar 10 (12.3) 5 (15.6) 5 (10.2) 0.505
        Peroneal 13 (16.0) 5 (15.6) 8 (16.3) 1.000
        Tibial 6 (7.4) 2 (6.3) 4 (8.2) 1.000
       CV slowinga 14 (17.3) 8 (25.0) 6 (12.2) 0.228
        Ulnar 10 (12.3) 6 (18.8) 4 (8.2) 0.182
        Peroneal 10 (12.3) 4 (12.5) 6 (12.2) 1.000
        Tibial 2 (2.5) 1 (3.1) 1 (2.0) 1.000
       Conduction blocka 8 (9.9) 3 (9.4) 5 (10.2) 1.000
        Ulnar 4 (4.9) 2 (6.3) 2 (4.1) 0.646
        Peroneal 8 (9.9) 3 (9.4) 5 (10.2) 1.000
        Tibial 2 (2.5) 2 (6.3) 0 (0.0) 0.153
       Decreased distal amplitudea 22 (27.2) 15 (46.9) 7 (14.3) 0.002b
        Ulnar 12 (14.8) 9 (28.1) 3 (6.1) 0.010b
        Peroneal 11 (13.6) 6 (18.8) 5 (10.2) 0.328
        Tibial 12 (14.8) 7 (21.9) 5 (10.2) 0.203
       Unexcitable nervesa 14 (17.3) 8 (25.0) 6 (12.2) 0.228
        Ulnar 5 (6.2) 5 (15.6) 0 (0.0) 0.008b
        Peroneal 12 (14.8) 7 (21.9) 5 (10.2) 0.102
        Tibial 8 (9.9) 7 (21.9) 1 (2.0) 0.005b
      SNAP
       Prolonged distal latencya 4 (4.9) 2 (6.3) 2 (4.1) 0.646
        Ulnar 3 (3.7) 2 (6.3) 1 (2.0) 0.559
        Sural 3 (3.7) 1 (3.1) 2 (4.1) 1.000
        Superficial peroneal 2 (2.5) 1 (3.1) 1 (2.0) 1.000
       CV slowinga 3 (3.7) 3 (9.4) 0 (0.0) 0.058
        Ulnar 2 (2.5) 2 (6.3) 0 (0.0) 0.153
        Sural 1 (1.2) 1 (3.1) 0 (0.0) 0.395
        Superficial peroneal 1 (1.2) 1 (3.1) 0 (0.0) 0.395
       Decreased distal amplitudea 6 (7.4) 1 (3.1) 5 (10.2) 0.395
        Ulnar 4 (4.9) 0 (0.0) 4 (8.2) 0.149
        Sural 1 (1.2) 1 (3.1) 0 (0.0) 0.395
        Superficial peroneal 1 (1.2) 0 (0.0) 1 (2.0) 1.000
       Unexcitable nervesa 20 (24.7) 13 (40.6) 7 (14.3) 0.009b
        Ulnar 12 (14.8) 6 (18.8) 6 (12.2) 0.526
        Sural 11 (13.6) 8 (25.0) 3 (6.1) 0.021b
        Superficial peroneal 9 (11.1) 6 (18.8) 3 (6.1) 0.144
      Late responses
       H-reflex 0.513
        Normal 11 (13.6) 3 (9.4) 8 (16.3)
        Bilaterally absent 70 (86.4) 29 (90.6) 41 (83.7)
       F-waves <0.001b
        Normal 45 (55.6) 9 (28.1) 36 (73.5)
        Prolonged/absent 36 (44.4) 23 (71.9) 13 (26.5)
      Pathophysiologic process
       Primary pathology 0.006b
        Equivocal 36 (44.4) 8 (25.0) 28 (57.1)
        Axonal or demyelinating 45 (55.6) 24 (75.0) 21 (42.9)
      Electromyography
       Abnormal spontaneous activitya 16 (19.8) 10 (31.3) 6 (12.2) 0.047b
        Increased insertional activity 11 (13.6) 8 (25.0) 3 (6.1) 0.023b
        PSW 11 (13.6) 7 (21.9) 4 (8.2) 0.105
        Fibrillations 9 (11.1) 7 (21.9) 2 (4.1) 0.026b
        Fasciculations 1 (1.2) 0 (0.0) 1 (2.0) 1.000
       Abnormal volitional MUAPsa 42 (51.9) 20 (62.5) 22 (44.9) 0.174
        Reduced recruitment 42 (51.9) 20 (62.5) 22 (44.9) 0.174
        Polyphasic MUAPs 1 (1.2) 0 (0.0) 1 (2.0) 1.000
        Increased duration 0 (0.0) 0 (0.0) 0 (0.0)
        Increased amplitude 0 (0.0) 0 (0.0) 0 (0.0)
        Abnormal configuration 0 (0.0) 0 (0.0) 0 (0.0)
      Complicated clinical course Total cohorta
      Any of the following complicated clinical course outcomes (respiratory failure and/or prolonged hospital stay)b 32 (39.5)
       Prolonged hospital stay only (≥15 days) 13 (16.1)
       Respiratory failure only (need for MV) 1 (1.2)
       Both respiratory failure and prolonged hospital stay 18 (22.2)
      Prolonged hospital stay (≥15 days)c 31 (38.3)
      Respiratory failure (need for MV)d 19 (23.5)
       Length of MV dependence among patients with respiratory failure (days) 10 (8 to 14)
      Without any of the complicated clinical course outcomes 49 (60.5)
      Parameter Univariate
      p-value Multivariate
      p-value
      Crude odds ratio (95% CI) Adjusted odds ratio (95% CI)
      Complicated clinical coursea (respiratory failure and/or prolonged hospital stay)
       Antecedent infection
        GI 4.00 (1.22 to 13.1) 0.022
       Clinical manifestations
        Marked motor deficits 4.78 (1.58 to 14.4) 0.006 10.21 (2.31 to 45.2) 0.002
        Cranial nerve deficits 16.47 (2.06 to 131.0) 0.008
        Dysautonomia 11.93 (3.06 to 46.5) <0.001 14.42 (2.16 to 96.1) 0.006
       CMAP
        Decreased distal amplitude 5.29 (1.84 to 15.3) 0.002
       SNAP
        Unexcitable nerves 4.11 (1.41 to 11.9) 0.009
       Late responses
        Prolonged/absent F-waves 7.08 (2.61 to 19.2) <0.001 8.00 (2.29 to 27.9) 0.001
       Primary pathology
        Demyelinating 3.50 (1.14 to 10.7) 0.029
        Axonal 4.67 (1.45 to 15.0) 0.010
       Abnormal spontaneous activity
        Increased insertional activity 5.00 (1.21 to 20.6) 0.026
        Fibrillations 6.44 (1.24 to 33.4) 0.026
      Respiratory failurea
       Clinical variant
        Classic sensorimotor GBS 3.75 (1.25 to 11.26) 0.018
       Clinical manifestations
        Dysautonomia 19.54 (5.30 to 72.1) <0.001 13.24 (3.17 to 55.4) <0.001
       CMAP
        Decreased distal amplitude 4.63 (1.54 to 13.9) 0.006
       Late responses
        Prolonged/absent F-waves 7.32 (2.16 to 24.8) 0.001 4.50 (1.14 to 17.8) 0.032
       Abnormal spontaneous activity
        Fibrillations 5.09 (1.21 to 21.4) 0.027
      Prolonged hospital staya
       Age (years) 1.03 (1.0003 to 1.06) 0.047
       Clinical manifestations
        Marked motor deficits 4.43 (1.46 to 13.4) 0.008 9.77 (2.18 to 43.7) 0.003
        Cranial nerve deficits 15.45 (1.94 to 123.0) 0.010
        Dysautonomia 12.90 (3.30 to 50.5) <0.001 15.33 (2.26 to 104.0) 0.005
       CMAP
        Decreased distal amplitude 5.76 (1.98 to 16.7) 0.001
       SNAP
        Unexcitable nerves 4.44 (1.52 to 12.9) 0.006
       Late responses
        Prolonged/absent F-waves 8.18 (2.94 to 22.8) <0.001 8.98 (2.51 to 32.1) 0.001
       Primary pathology
        Demyelinating 4.14 (1.31 to 13.1) 0.015
        Axonal 5.52 (1.67 to 18.2) 0.005
       Abnormal spontaneous activity
        Increased insertional activity 5.33 (1.29 to 22.0) 0.021
        Fibrillations 6.85 (1.32 to 35.6) 0.022
      Moderate-to-severe disability at discharge (GBS-DS 4-6)a
       Demographics
        Age (years) 1.07 (1.03 to 1.12) 0.001 1.07 (1.02 to 1.12) 0.006
       Clinical manifestations
        Dysautonomia 8.59 (2.41 to 30.6) 0.001 5.00 (1.12 to 22.4) 0.035
       CMAP
        Decreased distal amplitude 3.47 (1.05 to 11.4) 0.041
       Late responses
        Prolonged/absent F-waves 6.16 (1.57 to 24.22) 0.009
       Primary pathology
        Axonal 26.25 (3.0 to 229.0) 0.00 17.52 (1.31 to 234.0) 0.030
       Abnormal spontaneous activity
        PSW 5.56 (1.40 to 22.0) 0.015
        Fibrillations 8.61 (1.94 to 38.2) 0.005
      Table 1. Demographic and clinical features of the patients

      Values are presented as mean ± standard deviation, number (%), median (interquartile range). Mutually exclusive categories may not sum up to 100% because of rounding.

      URTI, upper respiratory tract infection; GI, gastrointestinal infections; UTI, urinary tract infection; GBS, Guillain-Barré syndrome; MFS, Miller-Fisher syndrome; MFS-GBS, Miller-Fisher syndrome and Guillain-Barre syndrome overlap; BP, blood pressure; HR, heart rate; CSF, cerebrospinal fluid; IVIg, intravenous immunoglobulin; PLEX, plasma exchange.

      Percentages may not sum up to the total because categories are not mutually exclusive.

      p < 0.05.

      Table 2. Findings from electromyography and nerve conduction studies of the patients

      Values are presented as mean±standard deviation or number (%). Mutually exclusive categories may not sum up to 100% because of rounding.

      EMG-NCS, electromyography and nerve conduction studies; CMAP, compound muscle action potential; CV, conduction velocity; SNAP, sensory nerve action potential; PSW, positive sharp waves; MUAP, motor unit action potential.

      Percentages may not sum up to the total because categories are not mutually exclusive.

      p < 0.05.

      Table 3. Prevalence of a complicated clinical course in the study cohort (n = 81)

      Values are presented as number (%) or median (interquartile range).

      MV, mechanical ventilation.

      Percentages do not sum up to 100% because categories are not mutually exclusive.

      Primary composite outcome

      With or without respiratory failure.

      With or without prolonged hospital stay.

      Table 4. Factors associated with a complicated clinical course and moderate-to-severe disability at discharge

      CI, confidence interval; GI, gastrointestinal infections; CMAP, compound muscle action potential; SNAP, sensory nerve action potential; GBS, Guillain-Barré syndrome; GBS-DS, Guillain-Barré syndrome disability scale; PSW, positive sharp waves.

      Variables with p > 0.05 were no longer included.

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