Abstract
Background: Pain in Guillain-Barré syndrome (GBS) may be pronounced and is often overlooked.
Objectives: To obtain detailed information about pain in GBS and its clinical variants.
Methods: This was a prospective cohort study in 156 patients with GBS (including 18 patients with Miller Fisher syndrome [MFS]). We assessed the location, type, and intensity of pain using questionnaires at standard time points during a 1-year follow-up. Pain data were compared to other clinical features and serology.
Results: Pain was reported in the 2 weeks preceding weakness in 36% of patients, 66% reported pain in the acute phase (first 3 weeks after inclusion), and 38% reported pain after 1 year. In the majority of patients, the intensity of pain was moderate to severe. Longitudinal analysis showed high mean pain intensity scores during the entire follow-up. Pain occurred in the whole spectrum of GBS. The mean pain intensity was predominantly high in patients with GBS (non-MFS), patients with sensory disturbances, and severely affected patients. Only during later stages of disease, severity of weakness and disability were significantly correlated with intensity of pain.
Conclusions: Pain is a common and often severe symptom in the whole spectrum of GBS (including MFS, mildly affected, and pure motor patients). As it frequently occurs as the first symptom, but may even last for at least 1 year, pain in GBS requires full attention. It is likely that sensory nerve fiber involvement results in more severe pain.
Guillain-Barré syndrome (GBS) is an acute immune-mediated polyradiculoneuropathy comprising a broad spectrum of clinical variants.1 Pain is often overlooked because most attention is given to progression of weakness. Various types of pain have been described in GBS.2 The pathophysiology of pain is poorly understood. The reported frequency of pain in GBS is highly variable, and most studies determined pain only in the acute phase of GBS (table e-1 on the Neurology® Web site at www.neurology.org).3,–,11 Two studies performed a longer follow-up and reported a decrease of pain intensity in time, and one-third of patients may even have pain after 2 years.4,8 Previously we showed that the character of pain may change during the clinical course of GBS.10 Pain has also been reported in patients with the Miller Fisher syndrome (MFS), acute motor axonal neuropathy (AMAN), and even mild forms of GBS.12,–,14 Pain may therefore be a severe and chronic problem in a considerable proportion of patients with GBS.
The frequency and nature of the pain in GBS, however, needs to be further defined. All studies thus far conducted included only a relatively small number of cases with a limited set of clinical, electrophysiologic, and serologic data. Moreover, neither the different types nor the different locations of pain were systematically analyzed. Here we report a prospective study defining the character, location, and intensity of pain in GBS during a follow-up of 1 year. In addition, detailed information regarding the clinical, electrophysiologic, and serologic phenotype was obtained to be able to relate the pain to the spectrum of GBS variants.
METHODS
Patients.
A total of 170 patients fulfilling the diagnostic criteria for GBS were prospectively included in the GBS Research about Pain and Heterogeneity (GRAPH) study.15,16 Exclusion criteria were age below 12 years and significant comorbidity with a worse prognosis (predicted survival less than 1 year). Patients with Bickerstaff encephalitis and patients who developed acute onset chronic inflammatory demyelinating polyneuropathy (A-CIDP) were also excluded.
Study design.
Patients were included in the GRAPH study in 55 participating Dutch centers between February 2005 and October 2008. The protocol was approved by the ethics committee of the participating centers. Clinical data, biological materials, and electrophysiologic data were collected systematically during 1-year follow-up, after obtaining written informed consent.
Questionnaires were filled in by the neurologist weekly during the hospital stay and once after 6 months. The first 3 weeks after inclusion was determined as the acute phase, because all included patients had their nadir of weakness within 3 weeks after inclusion. When the patient was discharged from the hospital, additional questionnaires were filled in by the patient at 3, 6, 9, and 12 months after inclusion. If questionnaires or answers to some questions appeared to be lacking after 1 week, our research coordinator phoned the patients and asked them to complete and return the questionnaires if possible. If the patient was not able to fill in the questionnaires, we asked relatives for help. Patients who sent back their questionnaires where some answers were missing were not excluded from the analyses.
Questionnaires.
Baseline characteristics and data about medical history were obtained. Medical history also included questions about the presence of chronic pain within 3 months before onset of GBS. If so, we asked for the type of pain and the daily use of analgesics. The first questionnaire also contained identical questions about pain in the 2 weeks before onset of weakness and pain since the onset of weakness. In all subsequent questionnaires, we asked about the presence of pain in the past week. Data about location ([low] back, interscapular, neck, extremities, and trunk) and type of pain (radicular pain, painful paresthesias and dysesthesias, joint pain, muscle pain, meningism, and other type of pain2) were also obtained. The reported pain had to be new or different from the pain felt in medical history. Intensity of pain was determined using an 11-point numerical rating scale (NRS), in which 0 represents no pain and 10 represents extreme pain.17 The character of pain was obtained based on the simplified version of the Dutch McGill Pain Questionnaire.18,19 The mean NRS of the severest pain in the past week was questioned. Additionally, pain intensity was classified into mild (NRS 0–4), moderate (NRS 5–7), and severe pain (NRS 8–10).20,21 The use of daily analgesics was obtained and categorized based on the WHO's pain ladder into the following categories: none, paracetamol or nonsteroidal anti-inflammatory drugs, opioids, antidepressants, or anticonvulsants.
Besides information about pain, neurologic symptoms and signs, impairment scales (Medical Research Council sumscore, ranging from 0 [quadriplegic] to 60 [normal strength],22 and Inflammatory Neuropathy Cause and Treatment [INCAT] sensory sumscore23,24), and disability scales (GBS disability score, ranging from 0 [no symptoms or signs] to 6 [dead],25 and overall disability sumscore [ODSS], ranging from 0 [no signs of disability] to 12 [most severe disability score]24,26), treatment and course of disease were obtained from the questionnaires filled in by the neurologist during the hospital stay and after 6 months. Regarding the INCAT sensory sumscore, we used the pinprick sensation score and vibration sensation score without the 2-point discrimination score, because this score was often missing.23,24
After hospital discharge, pain symptoms, Fatigue Severity Scale (FSS, ranging from 1 [no signs of fatigue] to 7 [most disabling fatigue]),27,28 disability scales (GBS disability score, ODSS), and course of disease were obtained from the questionnaires filled in by the patient.
Clinical autonomic functions were obtained over the last 7 days. Clinical autonomic dysfunction parameters were defined prior to study onset: hypertension (systolic >140 and/or diastolic >90 mm Hg), hypotension (systolic <90 mm Hg), tachycardia (heart rate >100 bpm), bradycardia (heart rate <60 bpm), gastrointestinal dysfunction (diarrhea, constipation, or incontinence), and bladder dysfunction (urine retention or incontinence).
We defined patients as GBS (non-MFS) or MFS when they fulfilled the diagnostic criteria.15,16 The pure motor variant was defined as having GBS without sensory deficits (normal pinprick and vibration sense). The GBS disability scale was used to indicate the severity of disease at nadir: mildly affected = able to walk unaided = GBS disability score ≤2; severely affected = unable to walk unaided = GBS disability score ≥3.
Preceding infections.
Clinical manifestations of infections within 3 weeks of onset of weakness were classified as influenza, influenza-like illness or respiratory tract infection, and gastroenteritis or diarrhea when these met the criteria of the Centers of Disease Control and Prevention definitions for nosocomial infections.29 Baseline serum samples were tested to determine recent infection with Campylobacter jejuni as described.30
Antiganglioside antibodies.
Pretreatment sera obtained after inclusion were tested for the presence of immunoglobulin G and immunoglobulin M antibodies against the gangliosides GM1, GM2, GD1a, and GQ1b using ELISA as described.31,32
Electromyographic studies.
Electrophysiologic investigations were scheduled within 3 weeks after inclusion. Investigations were executed according to local settings of the participating hospitals. Age- and sex-matched reference values were used.33 Electrophysiologic investigations were classified as demyelinating, axonal, inexcitable, equivocal, or normal.34
Statistics.
Percentages were compared between groups using the χ2 test or Fisher exact test if appropriate. Longitudinal analysis of pain intensity scores, allowing for occasional missing data at some time points, was performed using repeated-measurement analysis of variance in the total group and in subgroups using data from 2 weeks before onset weakness, the acute phase (inclusion day, 1, 2, and 3 weeks after inclusion), and the chronic phase (weeks 13, 26, 39, and 52 after inclusion). For the acute phase, we used the weekly data from the questionnaires until 3 weeks, because all patients had their nadir within 3 weeks after inclusion and after 3 weeks many patients had been discharged from the hospital, resulting in too small number of patients. The population of patients was divided into different subgroups, such as GBS (non-MFS) or MFS, and by age (using the median value as cutoff), sex, severity according to GBS disability scale (mildly or severely affected), sensory signs (pinprick and vibration sense), being treated with IV immunoglobulin (IVIg) with or without methylprednisolone (MP), electrophysiologic classification (demyelinating or axonal), and different infections. When there was no significant difference in the profile of mean values of the pain intensity score during the whole follow-up between the subgroups, we calculated the mean difference with 95% confidence interval between the subgroups from time before weakness until 52 weeks. Correlation between impairment (Medical Research Council sumscore, INCAT sensory sumscore), disability (GBS disability score, ODSS), and fatigue (FSS) vs pain intensity (NRS) was analyzed using Spearman rank correlation test (rs). For the relation between fatigue (FSS) and pain intensity (NRS), changes from the previous measurement were also evaluated using rs. All calculations were performed using SPSS for Windows 2000 (version 15.0, SPSS, Chicago). A 2-sided p value <0.05 was considered to be significant.
RESULTS
Patients.
Between February 2005 and October 2008, 170 patients with GBS were enrolled in the GRAPH study. During follow-up, some patients turned out to have another diagnosis (n = 3), Bickerstaff encephalitis (n = 2), an accompanying myelitis (n = 1), or A-CIDP (n = 8).35 These 14 patients were excluded from the analysis. Of the remaining 156 patients (61% male), 138 (88%) fulfilled the diagnostic criteria for GBS (non-MFS) and 18 (12%) had MFS.15,16
Patient characteristics.
Baseline and clinical characteristics, electrophysiologic classification, infections, and results of laboratory tests in the acute phase are listed in table 1. All patients had their nadir of weakness within 3 weeks after inclusion, and within 4 weeks after onset of weakness. At nadir, 81% of the patients (83% of GBS [non-MFS] and 67% of MFS) were unable to walk independently (severely affected). After 6 months, 11% of patients (12% of GBS [non-MFS] and 6% of MFS) were still unable to walk independently.
Baseline and clinical characteristics, electrophysiologic classification, infections, and antiganglioside antibodies in the acute phase in 156 patientsa
Pain.
Prevalence, location, type, and intensity of pain in the acute phase and during follow-up are listed in table 2. A total of 22% of patients had chronic pain in their medical history (mostly joint and backache, both 35%; nearly half of them [47%] used daily analgesics). A total of 66% of patients (69% of GBS [non-MFS] and 44% of MFS; p < 0.05) had pain in the acute phase. After the acute phase, the prevalence of pain between GBS [non-MFS] and MFS was not significantly different. A total of 36% of patients already had pain in the 2 weeks before the onset of weakness (40% of GBS [non-MFS] and 6% of MFS; p < 0.01; median 5 days, interquartile range 1–13). The prevalence of pain during the entire follow-up was significantly higher in patients with sensory disturbances compared to patients with the clinical pure motor form (t = 0: 62% vs 43%; t = 6 months: 56% vs 34%; p < 0.05). In the first 6 months, the prevalence of pain in mildly and severely affected patients was comparable; thereafter, the prevalence of pain was significantly higher in the severely affected patients (t = 39 weeks: 45% vs 17%, p < 0.01; t = 52 weeks: 42% vs 21%, p < 0.05). For the entire group, the prevalence of pain after 3, 6, and 9 months was significantly higher in patients with pain in the acute phase compared to patients without pain in the acute phase (p < 0.05). There was no significant difference in the prevalence of pain during the whole follow-up between the patients with or without chronic pain in medical history. From the patients having pain in the acute phase, 86% reported moderate to severe pain despite using analgesics. Mean pain intensity is shown in figure 1.
Presence, location, severity, and interpretation of pain in GBS (n = 156) and the use of daily analgesicsa
Mean pain intensity over time for the entire group (n = 156). Data shown are means (±SE) from analysis of variance. The means are based on number of patients (indicated in parentheses) with returned questionnaires and filled in numerical rating scale (NRS) score. Before weakness = maximum of 2 weeks before onset of weakness.
In the acute phase and during the entire period of follow-up, pain was most frequently present in the extremities. Low-back or back pain was notably present in the acute phase. Often, the patient indicated different types of pain at more than 1 location and the neurologist often indicated more than 1 interpretation (from the patients having pain, 61% reported pain at more than 1 location in the acute phase and 51% after 6 months; 53% had more than 1 interpretation for the pain in the acute phase and 31% after 6 months).
The mean pain intensity was higher in the acute and follow-up phase in females and patients with GBS (non-MFS), in patients with sensory disturbances, preceding gastroenteritis or diarrhea, and in severely affected patients (figure 2). No association was found between pain intensity and age, additional treatment with MP, the presence of antigangliosides, and demyelinating vs axonal GBS. When we excluded the patients with MFS to evaluate differences in the mean pain intensity between subgroups, the results were comparable (see figure 2 legend). Patients without pain before onset of weakness and patients without pain in the acute phase (n = 43) had a lower mean pain intensity in the beginning of the follow-up (week 13: mean difference −1.4 [−2.6, −0.2], p < 0.05; week 26: mean difference −1.3 [−2.6, −0.1], p < 0.05) compared to patients with pain during that period. This significant difference disappeared after 26 weeks.
Data shown are means (±SE) from analysis of variance. Mean differences (dotted minus solid line) in pain intensity (numerical rating scale [NRS]) with 95% confidence interval and p value; from time before onset of weakness to 52 weeks after onset of weakness between the different groups are indicated. (A) GBS (non-Miller Fisher syndrome [MFS]) (n = 138) and MFS (n = 18). (B) Weakness and sensory disturbances (n = 98) and pure motor (n = 52) (n = 6 unknown). Same analysis without MFS: mean difference in pain intensity = 0.9 (0.2, 1.7); p < 0.05. (C) Gastroenteritis or diarrhea (n = 52) and no gastroenteritis or diarrhea (n = 101) (n = 3 unknown). Same analysis without MFS: mean difference in pain intensity = −0.8 (−1.4, −0.1), p < 0.05. (D) Respiratory tract or influenza or influenza-like infection (n = 56) and no respiratory tract or influenza or influenza-like infection (n = 96) (n = 4 unknown). Same analysis without MFS: mean difference in pain intensity = 0.4 (−0.3, 1.1), p = 0.23. (E) Severely affected at nadir (n = 126) and mildly affected at nadir (n = 30). Same analysis without MFS: mean difference in pain intensity = 1.1 (0.2, 1.9), p < 0.05. (F) Female (n = 61) and male (n = 95). Same analysis without MFS: mean difference in pain intensity = 0.9 (0.3, 1.6), p < 0.01.
The correlation between disability, impairment, and fatigue vs pain intensity is listed in table 3. Summarized, pain intensity is associated with level of weakness, functional disability, and fatigue, not in the acute but during later stages of GBS. Sensory involvement is associated with the intensity of pain during the acute and later stage of GBS.
Correlations between disability, impairment, and fatigue in the chronic phase vs pain intensitya
DISCUSSION
This is the first large prospective follow-up study on the different aspects of pain in GBS in relation to the spectrum of GBS. As shown in this study, pain appeared to be a very common symptom in the acute phase and during the later stage of GBS and it also occurs in the whole spectrum of GBS variants, like MFS, pure motor, and mildly affected patients.
By far the most frequent location of pain during the entire follow-up was in the extremities, followed by low-back pain or back pain, and often more than one location was indicated. In MFS, neck pain occurred most frequently in the acute phase and also headache was regularly reported as other type of pain, which is also described in another study.13 This indicates that pain in GBS may affect various parts of the body. Comparing GBS (non-MFS) with MFS, the distribution of weakness seems to contribute to the distribution of pain.
Despite the use of analgesics, nearly half of the patients with pain reported moderate and one-third even severe pain. This emphasizes the magnitude of the clinical problem of pain in GBS. In a study in 55 patients with GBS, a similar mean pain intensity was found in the acute phase, but a lower mean pain intensity was found in the period until 24 weeks.8 We have asked for the presence of pain within 3 months before onset of weakness retrospectively, therefore recall bias may have affected this part of the results of our study. In the questionnaires, we emphasized that the reported pain during GBS had to be new or different from the pain felt in medical history. However, that it can be difficult for patients to differentiate between preexistent and new pain.
To identify factors that are associated with pain, we related pain to clinical features. As shown in this study, pain intensity is associated with level of weakness, functional disability, and fatigue, not in the acute but during later stages of GBS. Whether pain causes part of disability or disability contributes to pain cannot be concluded from our study. In another follow-up study, no significant correlation between disability and pain intensity was found.8 However, several years after GBS, an interaction between fatigue, pain, and muscle weakness has been described.36 In this study, they found a higher risk of pain and muscle weakness in individuals with pronounced fatigue. Both symptoms may influence each other and need to be registered. Depression or anxiety may also influence pain in GBS. Depression or anxiety was not specifically assessed in our study and needs further attention in forthcoming studies. Our results indicate that involvement of sensory nerves plays a role in the occurrence and intensity of pain during the acute and later stage of GBS. It has been described that years after GBS, muscle aches and cramps occur especially in patients with residual sensory disturbances.37 It was remarkable that in our study patients with previous diarrhea had a significantly higher mean pain intensity score compared to patients without diarrhea. The fact that in this study the number of pure motor patients or severely affected patients was not significantly different in the group with and without diarrhea does not explain the difference. Possibly different immunologic factors generated by an infection may play a role in pain.
The pathophysiology of pain in GBS is largely unknown and this study indicates the complexity of studying pain in GBS. Affected nerve roots may explain the occurrence of radicular nociceptive nerve pain affecting the low back or back with radiation to extremities or trunk.5 Inflammatory factors generating pain via the nervi nervorum may also play a role in the pathophysiology of pain, but has not been studied yet. In our study, the prevalence of back pain was higher than the prevalence of radicular pain, indicating that other types of pain like muscle pain or arthralgia possibly due to immobilization may also contribute to back pain in GBS. Neuropathic pain due to spontaneous or abnormal activity from large myelinated sensory afferents may explain the occurrence of painful paraesthesias and dysesthesias in the extremities. However, considering the high prevalence of pain in the extremities, other types of pain also may play a role. Small nerve fibers can also be affected in GBS.38 Affected small nerve fibers in GBS may play a role in pain and autonomic dysfunction and needs additional studies.
Nevertheless, 2 different combinations of pain symptoms may be distinguished. One combination starts before onset of weakness until hospital discharge, is mostly located in the extremities, and contains especially radicular pain, painful paresthesiae, and muscle pain; the other combination is predominantly present after hospital discharge during rehabilitation, is also mostly located in the extremities, and contains especially painful paresthesiae, muscle pain, and arthralgia. The intensity of pain is severe during the course of disease, but is most severe in the acute phase. Pain symptoms are associated with sensory disturbances and severe pain symptoms later in the stage of disease are associated with a higher level of weakness and disability. Patients with acute pain symptoms have a higher change on the occurrence of the pain symptoms in the later stage.
In case reports, the analgesic effect of corticosteroids for lumbar and leg pain has been described.39,40 In this study there appeared to be no difference in pain between patients treated with MP or not, which is in line with a previous study on the additional effect of MP in GBS.10
AUTHOR CONTRIBUTIONS
Statistical analysis was conducted by Dr. W.C.J. Hop and Dr. L. Ruts.
COINVESTIGATORS
The Dutch GBS Study Group (neurologists, including and assessing patients with GBS, who contributed to the study): L. Ruts, MD, and P.A. van Doorn, PhD, MD (Erasmus MC, Rotterdam, n = 33); A.J. van der Kooi, PhD, MD (AMC, Amsterdam, n = 10); G.W. van Dijk, PhD, MD (Canisius-Wilhelmina, Nijmegen, n = 10); H.A.W. Sinnige, MD (Maasstad ZH, locatie Clara & Zuider, n = 12); F.H. Vermeij, MD (SFG, Rotterdam, n = 10); U.A. Badrising, PhD, MD (Bethesda ZH, Middelharnis, n = 8); I.N. van Schaik, PhD, MD (OLVG, Amsterdam, n = 7); J.C.B. Verhey, MD (Vlietland ZH, Schiedam, n = 7); J.S. Straver, MD (Hofpoort ZH, Woerden, n = 6); W.H.J.P. Linssen, PhD, MD (Lucas Andreas ZH, Amsterdam, n = 5); E.G.J. Zandbergen, MD (ZH Rijnstate, Arnhem, n = 4); M.C. de Rijk, PhD, MD (Catharina-ZH, Eindhoven, n = 4); W.L. van der Pol, PhD, MD (UMCU, Utrecht, n = 4); J.P. Blankevoort, PhD, MD (Flevo ZH, Almere, n = 3); D.G. Oenema, MD (Wilhelmina ZH, Assen, n = 3); B. Feenstra, MD (Lievensberg ZH, Bergen op Zoom, n = 3); D.J. Hofstee, MD (St. Jansdal ZH, Harderwijk, n = 3); R. Beekman, PhD, MD (Atrium MC, Heerlen, n = 3); C.G. Faber, PhD, MD (UMCM, Maastricht, n = 3); R.A.I.A.M. Bernsen, PhD, MD (Jeroen Bosch ZH, Den Bosch, n = 3); W.G.H. Oerlemans, MD (Meander MC, Amersfoort, n = 2); R.W.M. Keunen, PhD, MD (HAGA ZH loc. Leyenburg, Den Haag, n = 2); G.H.M. Verheul, MD (Groene Hart ZH, Gouda, n = 2); W. Snoek, PhD, MD (Martini ZH, Groningen, n = 2); T.C. van der Ree, MD (Westfries Gasthuis, Hoorn, n = 2); W.J. Schuiling, MD (MC Leeuwarden, Leeuwarden, n = 2); J.L.M. Jongen (Ruwaard van Putten ZH, Spijkenisse, n = 2); Dr. L.H. Visser (Sint Elisabeth ZH, Tilburg, n = 2); G.M.J. Lassouw (VieCuri MC, Venlo, n = 2); Dr. V.I.H. Kwa, PhD, MD (Slotervaart ZH, Amsterdam, n = 1); J.A. Don, MD (Delfzicht ZH, Delfzijl, n = 1); M.J.B. Taphoorn, PhD, MD (HAGA ZH loc. Westeinde, Den Haag, n = 1); F. Visscher, MD (St. Oosterschelde ZH, Goes, n = 1); R.J.W. Witteveen, MD (Rijnland ZH, Leiderdorp, n = 1); J.J.G.M. Verschuuren, PhD, MD (LUMC, Leiden, n = 1); E.M. Leenders, MD (IJsselmeer ZH, Lelystad, n = 1); P.H.M.F. van Domburg, PhD, MD (Laurentius ZH, Roermond, n = 1); D.M.H. Zuidgeest, MD (Ikazia ZH, Rotterdam, n = 1); H.J. Vroon, MD (Haven ZH, Rotterdam, n = 1); R.J. Groen, MD (Lange Land ZH, Zoetermeer, n = 1).
DISCLOSURE
Dr. Ruts reports no disclosures. Dr. Drenthen receives research support from the Prinses Beatrix Fonds. Dr. Jongen has received speaker honoraria from Pfizer Inc., Johnson & Johnson, and Boehringer Ingelheim; and has received research support from the Dutch Ministry of Health. Dr. Hop and Dr. Visser report no disclosures. Dr. Jacobs has received research support from the Netherlands Organization for Health Research and Development, Erasmus MC, the Prinses Beatrix Fonds, and GBS-CIDP Foundation International. Prof. Dr. van Doorn has served on scientific advisory boards for Octapharma AG and Talecris Biotherapeutics; received a speaker honorarium from Baxter International Inc.; and serves on the editorial board of the Journal of the Peripheral Nervous System.
ACKNOWLEDGMENT
The authors thank the patients for taking part in the study; the coinvestigators of the Dutch GBS Study Group listed in the appendix; Drs. K. Kuitwaard, M.L. Kuijf, and S.I. van Nes, residents in Neurology (Erasmus MC, Rotterdam), and Dr. R. van Koniningsveld (currently working in Elkerliek ziekenhuis, Helmond) for including patients; and A.P. Tio-Gillen for determining the antiganglioside antibodies (Erasmus MC, Rotterdam) and M.M. de Kimpe, administrative coordinator, GRAPH study (Erasmus MC, Rotterdam).
Footnotes
-
- A-CIDP
- acute onset chronic inflammatory demyelinating polyneuropathy
- AIDP
- acute inflammatory demyelinating polyneuropathy
- AMAN
- acute motor axonal neuropathy
- CMAP
- compound muscle action potential
- DML
- distal motor latency
- FSS
- Fatigue Severity Scale
- GBS
- Guillain-Barré syndrome
- GRAPH
- GBS Research about Pain and Heterogeneity
- INCAT
- Inflammatory Neuropathy Cause and Treatment
- IVIg
- IV immunoglobulin
- MFS
- Miller Fisher syndrome
- mNCV
- motor nerve conduction velocity
- MP
- methylprednisolone
- NRS
- numerical rating scale
- ODSS
- overall disability sumscore
- SNAP
- sensory nerve action potential
- sNCV
- sensory nerve conduction velocity
Editorial, page 1406
Supplemental data at www.neurology.org
- Received January 30, 2010.
- Accepted June 29, 2010.
- Copyright © 2010 by AAN Enterprises, Inc.
REFERENCES
Letters: Rapid online correspondence
REQUIREMENTS
If you are uploading a letter concerning an article:
You must have updated your disclosures within six months: http://submit.neurology.org
Your co-authors must send a completed Publishing Agreement Form to Neurology Staff (not necessary for the lead/corresponding author as the form below will suffice) before you upload your comment.
If you are responding to a comment that was written about an article you originally authored:
You (and co-authors) do not need to fill out forms or check disclosures as author forms are still valid
and apply to letter.
Submission specifications:
- Submissions must be < 200 words with < 5 references. Reference 1 must be the article on which you are commenting.
- Submissions should not have more than 5 authors. (Exception: original author replies can include all original authors of the article)
- Submit only on articles published within 6 months of issue date.
- Do not be redundant. Read any comments already posted on the article prior to submission.
- Submitted comments are subject to editing and editor review prior to posting.
You May Also be Interested in
More Online
Hemiplegic Migraine Associated With PRRT2 Variations A Clinical and Genetic Study
Dr. Robert Shapiro and Dr. Amynah Pradhan