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Neurology India
Medknow Publications on behalf of the Neurological Society of India
ISSN: 0028-3886 EISSN: 1998-4022
Vol. 59, Num. 5, 2011, pp. 712-716

Neurology India, Vol. 59, No. 5, September-October, 2011, pp. 712-716

Topic of the Issue: Original Article

Temporal profile of pain and other sensory manifestations in Guillain-Barre' syndrome during ten days of hospitalization

K Karkare1, Arun B Taly1, Sanjib Sinha1, S Rao2

1 Department of Neurology, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, India
2 Department of Biostatistics, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, India
Correspondence Address: Arun B Taly, National Institute of Mental Health and Neurosciences (NIMHANS), Hosur Road, Bangalore - 560029, India,

Date of Submission: 22-Aug-2011
Date of Decision: 30-Aug-2011
Date of Acceptance: 18-Sep-2011

Code Number: ni11216

PMID: 22019656

DOI: 10.4103/0028-3886.86546


Background: Focused studies on sensory manifestations, especially pain and paresthesia in Guillain-Barre' (GB) syndrome are few and far between.
Aim: To study the sensory manifestations in GB syndrome during 10 days of hospitalization with clinico-electrophysiological correlation.
Materials and Methods:
The study included 60 non-consecutive patients with GB syndrome, fulfilling National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) criteria for GB syndrome. Data especially related to clinical and electrophysiological evidence of sensory involvement were analyzed. Pain was assessed using a) visual analogue paraesthesias (Vapar), b) visual analogue for pain (Vap) and c) verbal rating scale for pain (Verp).
Sensory symptoms were widely prevalent: paraesthesia in 45 (75%) patients and pain in 30 (50%) patients. Impairment of different sensory modalities included: pain in 8 (13.3%), joint position sense in 14 (23.3%), and vibration in 11 (18.3%). Electrophysiological evidence of abnormal sensory nerve conduction was noted in 35 (58.3%) patients. Pain assessment using Vapar, Vap and Verp for from Day 1 to Day 10 of hospitalization revealed that from Day 7 onwards the degree and frequency of sensory symptoms and signs decreased. On comparing various clinico-electrophysiological parameters among patients of GB syndrome with and without pain and paresthesia. Presence of respiratory distress correlated with pain and paresthesia (P=0.02).
Conclusions: Sensory manifestations in GB syndrome are often under-recognized and under-emphasized. This study analyzed the evolution and the profile of pain and paresthesia in GB syndrome during hospitalization. Knowledge, especially about evolution of pain and paresthesia during hospitalization might improve understanding and patient care.

Keywords: Guillain-Barre syndrome, pain, paresthesia, sensory symptoms


In 1916, Guillain, Barre', and Strohl emphasized motor weakness, areflexia, paraesthesias with slight sensory loss, and increased protein in cerebrospinal fluid (CSF) with no pleocytosis as important manifestations of the Guillain-Barre' syndrome (GBS). Disability due to motor weakness is responsible for morbidity in GBS. Though subjective sensory symptoms are common, severe sensory impairment is uncommon and is often overshadowed by motor weakness. Studies of sensory system involvement and pain in particular in patients with GBS are few and far between. [1],[2],[3],[4],[5] Moreover the evolution of these symptoms in the acute phase of the illness has not been evaluated. In this study we planned to study the sensory manifestations, in particular its temporal profile in patients with GBS during their 10 days of hospitalization with clinico-electrophysiological correlation.

Materials and Methods

The study was a descriptive hospital-based study conducted at the Department of Neurology, NIMHANS, Bangalore, between September 2008 and December 2009. Sixty non-consecutive patients with GBS in the age group of 16-65 years fulfilling National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) criteria for GBS were included. [6] Patients with respiratory involvement at the time of first evaluation as assessed by single breath count of less than 20 were excluded. The study was approved by the Institutional Ethics Committee. Informed consent was obtained from the patients or the accompanying relatives.

Patients were initially evaluated in the Emergency Department and subsequently shifted or transferred to in-patient services. Data was collected on 10 consecutive days from the day of admission. The first questionnaire was administered within the first 48 hour of admission. Information was collected in a pre-designed proforma. Demographic data with regards to age, gender, and educational status was recorded. Enquiry about GBS included duration of illness, presence and location of paraesthesia/pain, weakness, history of antecedent factors if any, and history of autonomic disturbances. Examination included measurement of blood pressure in supine and sitting position whenever possible, single breath count, chest expansion and neurological examination. Investigations done included: complete hemogram, serum biochemistry including creatine phosphokinase (CPK) and potassium, serology for rheumatoid arthritis factor (RA), anti-nuclear antibody (ANA), Hepatitis B surface antigen (HBsAg), and human immunodeficiency virus (HIV), urine for porbhobilinogen and Bence Jones protein and CSF studies.

Pain and paresthesia were measured using the Wong and Baker Face scale. Patients were explained about the scale and were required to give a score separately each for pain and paresthesia. [7] Verbal rating scale was also used with 0 being no pain and 10 severe pain.

All patients underwent conventional electrodiagnostic studies: right median and ulnar motor and sensory conduction studies including F waves and lower limb common peroneal and sural nerve conduction studies. Conduction parameters were considered abnormal if they were beyond 20% of the upper or lower limits of laboratory values of healthy controls. Patients were categorized according to Hadden's criteria as primary demyelinating, axonal, inexcitable, equivocal and normal with emphasis on sensory conduction parameters. [8] Patients received symptomatic treatment with either non-steriodal anti-inflammatory drugs (NSAIDs) or anti-neuralgic medications like carbamazepine, amytriptiline, gabapentin and pregabalin. All patients underwent specific treatment with five plasma exchanges on alternate days (40-50 ml/kg).

Statistical analysis

Data was expressed using descriptive statistics for continuous variables and frequency and percentage for categorical variables. Comparison between clinical variable groups and continuous variables was done using independent sample't' test or ANOVA as appropriate. Association between categorical variables was established by Chi Square test or Fisher's exact test. Values of p0 <0.05 were considered statistically significant.


The cohort consisted of 60 patients with mean age 32.75 ± 12.9 years (range 16-65 years; median: 30), and 46 (76.7%) men and 14 (23.3%) women. Thirty-four (56.7%) patients presented in the first week of illness, 15 (25%) in second week, and 11 (18.3%) patients in the third week. Eleven (18.33%) patients were in the progressive phase of illness at presentation. Antecedent events were observed in 40 (66.7%) patients and included fever (70%), diarrhea (30%), respiratory symptoms (12.5%) and others (15%).

Clinical profile

Historically, 54 (90%) patients had distal weakness of upper limb, 56 (93.3%) had distal weakness of lower limb, and 46 (76.7%) patients had proximal weakness of upper limb, while 55 (91.7%) patients had proximal weakness of lower limb. Sensory symptoms were widely prevalent: paresthesia in upper limb in 40 (66.6%) patients, paresthesia in lower limb in 43 (71.6%) patients, and pain in 30 (50%) patients. Bulbar symptoms were present in 23 (8.33%) patients and included: dysphagia in nine (15%), poor cough in eight (13.3%), dysphonia in seven (11.7%), and drooling in six (10%). One patient (1.7%) needed nasogastric feeding. Autonomic symptoms were present in 10 (16.6%) patients: dry mouth -4, increased sweating -3, constipation -3, cold feet-1, and hesitancy to pass urine -1. General examination revealed: pallor (eight, 13.3%), lymphadenopathy (two, 3.3%), and clubbing (two, 3.3%). Cranial nerve examination revealed facial palsy in 23 (38.3%) and papilledema in two (3.3%). Sensory impairment was noted in the following modalities: pain in eight (13.3%), joint position sense in 14 (23.3%), and vibration in 11 (18.3%) [Table - 1]. Four patients (6.6%) had brisk stretch reflexes. The severity of disability by Hughes score and Modified Rankins score is shown in [Table - 2].

The ESR at 1 st hour ranged from - 1 to 96 mm/hour (mean 25.84 ± 24.10, median-15). The serum CPK values ranged from 32 to 1688 IU/L (mean: 372 ± 415, median-197). The CSF cell count varied from 0 to 7 cells/cu mm (mean: 1.55 ± 2.96) and protein ranged from 22 to 630 mg/dl (mean: 151.73 ± 130.40, median-114). Electrophysiological sensory abnormalities in median, ulnar and sural nerves were noted in 27, 31 and 17 patients respectively, suggesting an 'abnormal median and normal sural' (AMNS) response. Overall this pattern was detected in 35 (58.3%) of patients.

The distribution of pain, paresthesia, use of anti-neuralgesics and painkillers; visual analogue for paresthesias (Vapar), visual analogue for pain (Vap) and verbal rating scale for pain (Verp) from Day 1 to Day 10 of hospitalization are given in [Table - 3] and [Figure - 1]. It is interesting to note that from Day 7 onwards the degree and frequency of sensory symptoms and signs decreased. On comparing various parameters among patients with GBS with and without pain and paresthesia, the only statistically significant difference was the presence of respiratory involvement in those with pain and paresthesia (P=0.02). None of the other factors were significant [Table - 4].


The GB syndrome is one of the severe forms of polyneuropathies with variable sensory symptoms, motor disability, need for hospitalization and uncertainty of the course of the disease. The phenotypic description otherwise is similar to the reported literature. [3],[9],[10],[11],[12]

Sensory disturbances, especially pain, are common in GBS. However, there are only few focused studies in the literature about the pain disturbances in GBS. In this study sensory symptoms, paresthesias and pain were widely prevalent and both pain and paresthesia was evident in 80% of the patients. Sensory symptoms were more frequent in the lower limbs suggesting a length-dependent phenomenon. The possible reasons for the increased prevalence of sensory symptoms in this study could be due to two factors: daily evaluation for ten consecutive days from the day of admission and specific enquiry about sensory manifestations. Though GBS is dominated by motor weakness sensory dysfunction may cause pain, impaired quality of life, and even poor sleep. In this study it is of interest to note that from Day 7 onwards, the degree and frequency of sensory symptoms and signs decreased. There is no study documenting objectively sensory symptoms and signs for 10 consecutive days during hospitalization. The sensory dysfunction matched with the motor deficits. The improvement in sensory symptoms from Day 7 could be due to both specific and symptomatic treatment during the hospitalization. Takeuchi et al., [2] had reported increased frequency of residual deficits in patients with kinesthetic impairment. Therefore sensory dysfunction in GB syndrome has a prognostic role as well. Detection of sensory dysfunction clinically has been reported to vary between 59% and 66%. [3],[12],[13] Ruts et al., [4] recently described 156 patients with GB syndrome and reported pain two weeks preceding weakness in 36% of patients, in 66% of patients in the acute phase (first three weeks after inclusion), and in 38% of patients after one year.On comparing various parameters among patients with GBS with and without sensory manifestations, pain and paresthesia, the only statistically significant difference was presence of respiratory involvement in those with pain and paresthesia (P=0.02). It can be conjectured that this correlation suggests that the severity and extent of nerve fiber involvement may dictate this association, nevertheless our study did not find a correlation between sensory symptoms and severity of the illness.

Electrophysiological evidence of sensory dysfunction has been reported from 60-96% of the tested nerves. [3],[13] However, in this study the evidence of sensory involvement was similar both clinically and electrophysiologically. This may be related to early performance of nerve conduction studies, patchy involvement of sensory nerve fibers, and involvement of small-diameter fibers. The upper limb sensory nerves, median and ulnar, were more often involved than the lower limb sensory sural nerve. This "abnormal median and normal sural (AMNS)" pattern noted in this study had been previously well-documented in GBS. [3],[13],[14],[15],[16] This AMNS pattern is attributed to the sural nerve being free of entrapment as compared to the median nerve. Further, the distal sensory nerve might be more involved in GBS and the sural is recorded more proximally. This hypothesis is supported by more involvement of ulnar nerves in this study. Recently, the importance of small fibers in the generation of pain has been reported by Martinez et al. [5]

In the current study, the patients recruited were not critically ill as this might have hampered their participation in a questionnaire-based enquiry. Another limitation was non-consecutive selection of subjects depending on the feasibility of evaluation by the investigator. Further, patients were admitted on different days of their illness as is observed in the majority of the studies involving GBS. [1],[3] The electrophysiological studies were carried out early and on variable days of hospitalization.


1.Cornblath DR, Mellits ED, Griffin JW, McKhann GM, Albers JW, Miller RG, Feasby TE, Quaskey SA. Motor conduction studies in GB syndrome and its prognostic values. Ann Neurol 1988;23:354-9.   Back to cited text no. 1    
2.Takeuchi H, Takahashi M, Kang J, Ueno S, Yamada A, Miki H, Tarui S. The Guillain-Barré syndrome: Clinical and electroneuromyographic studies. J Neurol 1984;231:6-10.   Back to cited text no. 2    
3.Taly AB, Veerendrakumar M, Das KB, Gupta SK, Suresh TG, Rao S, et al. Sensory dysfunction in GB syndrome: A clinical and electrophysiological study of 100 patients. Electromyogr Clin Neurophysiol 1997;37:49-54.   Back to cited text no. 3    
4.Ruts L, Drenthen J, Jongen JL, Hop WC, Visser GH, Jacobs BC, et al. Pain in Guillain-Barre syndrome: A long-term follow-up study. Neurology 2010;75:1439-47.   Back to cited text no. 4    
5.Martinez V, Fletcher D, Martin F, Orlikowski D, Sharshar T, Chauvin M, et al. Small fibre impairment predicts neuropathic pain in Guillain-Barré syndrome. Pain 2010;151:53-60.  Back to cited text no. 5    
6.Asbury AK, Cornblath DR. Assessment of current diagnostic criteria for Guillain-Barré syndrome. Ann Neurol 1990;27 (Suppl):S21-4.  Back to cited text no. 6    
7.Garra G, Singer AJ, Taira BR, Chohan J, Cardoz H, Chisena E, et al. Validation of the Wong-Baker FACES Pain Rating Scale in pediatric emergency department patients. Acad Emerg Med 2010;17:50-4.   Back to cited text no. 7    
8.Hadden RD, Cornblath DR, Hughes RA, Zielasek J, Hartung HP, Toyka KV, et al. Electrophysiological classification of Guillain-Barré syndrome: Clinical associations and outcome. Plasma Exchange/Sandoglobulin Guillain-Barré Syndrome Trial Group. Ann Neurol 1998;44:780-8.  Back to cited text no. 8    
9.Moulin DE, Hagen N, Feasby TE, Amireh R, Hahn A. Pain in Guillain-Barre´syndrome. Neurology 1997;48:328-31.  Back to cited text no. 9    
10.Pentland B, Donald S. Pain in the Guillain-Barré syndrome: A clinical review. Pain 1994;59:159-64.   Back to cited text no. 10    
11.Winer JB, Hughes R, Osmond C. A prospective study of acute idiopathic neuropathy. I. Clinical features and their prognostic value. J Neurol Neurosurg Psychiatry 1988;51:605-12.   Back to cited text no. 11    
12.Govoni V, Granieri E. Epidemiology of Guillain Barre syndrome. Curr Opin Neurol 2001;14:605-13.  Back to cited text no. 12    
13.Ropper AH, Wijdicks EF, Shahani BT. Electrodiagnostic abnormalities in 113 consecutive patients with Guillain-Barré syndrome. Arch Neurol 1990;47:881-7.   Back to cited text no. 13    
14.Kaur U, Chopra JS, Prabhakar S, Radhakrishnan K, Rana S. Guillain-Barré syndrome. A clinical electrophysiological and biochemical study. Acta Neurol Scand 1986;73:394-402.  Back to cited text no. 14    
15.Bromberg MB, Albers JW. Patterns of sensory nerve conduction abnormalities in demyelinating and axonal peripheral nerve disorders. Muscle Nerve 1993;16:262-6.   Back to cited text no. 15    
16.Fraser JL. Distal sensory fiber involvement in inflammatory demyelinating polyneuropathies. Muscle Nerve 1994;17:112-3.  Back to cited text no. 16    

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