Guillain-Barre Syndrome (GBS) is an acute, immune-mediated polyradiculoneuropathy characterized by rapidly progressive, symmetrical limb weakness, areflexia, and varying degrees of sensory and autonomic dysfunction. Since the global eradication of Poliomyelitis in many parts of the world, GBS has emerged as the most common cause of acute flaccid paralysis across all age groups  (Willison et al, 2016). ^[1]

The global incidence of GBS ranges from 1.1 to 1.8 per 100,000 population per year, with reported mortality between 3–7%. In India, the incidence varies from 0.4 to 4.0 per 100,000 population annually (Anita Mcgrogan et al,2009). ^[2]. Despite advances in intensive care and immunotherapy, approximately 20–30% of patients experience severe disability during the acute phase, and 10–15% are left with long-term residual disabilities. [3]. Also  it show high inflammatory response resulting in an increase in CRP and ESR (Vaishnavi et al, 2014). ^[4]

GBS is primarily autoimmune in origin and is frequently preceded by respiratory or gastrointestinal infections. Molecular mimicry between microbial antigens and peripheral nerve components triggers an aberrant immune response directed against myelin or axonal membranes. This immune-mediated inflammatory cascade results in demyelination, axonal degeneration, or both, depending on the subtype of GBS. The two major electrophysiological subtypes include acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN), each demonstrating distinct pathological and prognostic characteristics.

Inflammation plays a pivotal role in the pathogenesis and progression of GBS. Elevated inflammatory markers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) reflect systemic immune activation. Increased levels of these markers have been associated with heightened inflammatory activity and may correlate with disease severity and progression. CRP, an acute-phase reactant synthesized by the liver in response to pro-inflammatory cytokines such as interleukin-6 (IL-6), serves as a sensitive indicator of systemic inflammation. Similarly, ESR is a nonspecific marker that reflects the presence of inflammatory proteins in plasma. Previous studies have suggested that elevated CRP and ESR levels may be associated with more severe clinical presentations and poorer outcomes in GBS patients. Recent advances in medical research have illuminated the role of inflammatory markers and nerve-conduction studies in the diagnosis and monitoring of GBS. Elevated inflammatory markers, such as C-reactive protein (CRP) and interleukin-6 (IL-6), are often associated with systemic inflammation and may reflect the extent of the autoimmune response driving the neuropathy.

Conversely, nerve-conduction studies (NCS) constitute a cornerstone in the diagnostic evaluation of GBS and are essential for determining the subtype and severity of nerve involvement. These electrophysiological assessments measure parameters such as conduction velocity, distal latency, amplitude of compound muscle action potentials (CMAP), and sensory nerve action potentials (SNAP). Findings may reveal demyelinating features—such as prolonged distal latencies and slowed conduction velocities—or axonal degeneration characterized by reduced amplitude or absent motor and sensory responses. Furthermore, the preferential sparing of sural sensory nerve action potential (SNAP) is seen in almost half of GBS patients.[^5,6,7] The extent of abnormalities detected on NCS often correlates with clinical severity, functional impairment  providing valuable insights into the extent of nerve involvement and aiding in the prediction of disease progression.

Currently, there is no single definitive biomarker for GBS, and diagnosis relies on a combination of clinical evaluation, cerebrospinal fluid (CSF) analysis demonstrating albuminocytological dissociation, and electrophysiological studies. Given the variability in clinical course—from mild weakness to respiratory failure requiring mechanical ventilation—early identification of prognostic indicators is crucial for risk stratification and therapeutic decision-making. Therefore, this research aims to evaluate the relationship between clinical severity of GBS and inflammatory markers (CRP and ESR), along with nerve-conduction study findings. By correlating biochemical and electrophysiological parameters with disability grading, this research seeks to improve prognostic assessment and contribute to more targeted and timely management strategies in patients with GBS.

AIM & OBJECTIVES: -

AIM: The aim of this study is to evaluate the clinical severity of Guillain–Barré Syndrome (GBS) in relation to serum inflammatory markers (CRP and ESR) and findings from nerve conduction studies.

OBJECTIVES:

1. To measure serum inflammatory markers, specifically C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), in patients diagnosed with GBS.
2. To assess motor and sensory nerve conduction study (NCS) parameters in these patients.
3. To determine the clinical severity of GBS using the Hughes disability scale.
4. To analyse the correlation between inflammatory marker levels and NCS findings with the clinical severity of GBS.

MATERIALS & METHODS-

This was a cross-sectional study carried out in the Department of Neurology, in collaboration with the Department of Physiology and the Department of Medicine at VIMSAR, Burla. The study was conducted from June 2022 to December 2024. The study was conducted after obtaining approval from the Institutional Ethics Committee, and written informed consent was obtained from each participant prior to inclusion in the study. A total of 61 patients of both sexes who were clinically diagnosed with Guillain–Barré Syndrome (GBS) were included in the study. The sample size was calculated using the Rosoft sample size calculator.

Patients presenting with progressive weakness of both limbs, relative symmetry of symptoms, decreased or absent tendon reflexes, sensory symptoms or signs, and bilateral cranial nerve involvement (mostly facial muscle weakness) were included in the study according to the diagnostic criteria described as per as per Asbury and Cornblath (1990) ^[8] .

Patients were excluded if they had other neurological illnesses that could affect nerve conduction studies (such as diabetes mellitus, drug- or toxin-induced neuropathy), pregnant women, patients with tumors or those receiving immunomodulatory therapy, patients with systemic failure (respiratory, renal, hepatic, or cardiac), and patients with severe psychiatric illness.

After inclusion, all patients underwent laboratory and electrophysiological evaluation. Serum C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were measured in each patient. Nerve conduction studies (NCS), including both motor and sensory nerve conduction as well as F-wave study of the median nerve, were performed. The study tools used included the turbidimetry method for estimation of CRP, the Westergren method for ESR measurement, and the Medicaid Neurostim system for nerve conduction studies. Clinical severity of GBS was assessed using the Hughes and Rees disability scale.

CLINICAL SEVERITY- (Hughes & Rees scale (1997) ^[9]

1. healthy
2. minor symptoms, capable of running
3. able to walk without assistance, unable to run
4. able to walk with help
5. Chair bound/bedridden

5.requiring ventilation for at least part of the day

6. Dead

All the relevant DATA were collected in a predesigned proforma. Statistical analysis was done by using SPSS software. ANOVA test was applied and p-value <0.05 was considered significant

RESULTS:

In the present study, total number of patients included were sixty (60) out of which 41 were male and 19 were female belonging to the age group 15 to 45 years. The table-1 shows the demographic data of all the study participants. In this study, we also observed that 34 patients (56.6%) presented with URTI as the most common predisposing factor. Also all the participants presented with neurological symptoms (both sensory & motor). However only 6 patients (10% cases) required mechanical ventilation.    

Table-1

In this study, all the study participants were categorized into 5 grades based on clinical severity as per the Hughes & Rees scale. Out of 60 participants, 4 patients belonged to grade-1, 9 patients grade-2, 17 patients grade-3, 25 patients grade-4 and only 5 patients belonged to grade-5.

When we compared serum CRP level in different grades of patients as shown in figure -1, we found that the level was significantly raised in grade 4 and grade 5 group of patients that is 15mg/dl and 18mg/dl respectively (p < 0.001). However, when we compared ESR level with clinical severity grades as shown in figure-2, we observed that grade -4 patients had  high ESR level i.e 31.33mm in 1^st hour which was significant (p < 0.001) .

Figure-1: Mean serum CRP level (mg/dl) and clinical severity grades

Figure-2: Mean ESR (mm/ 1st hr) level and clinical severity grades

When motor nerve conduction study was performed and its result was compared with CRP level as shown in figure-3 and figure-4, raised CRP level was positively associated with nerve conduction abnormalities in median nerve and common peroneal nerve of GBS patients respectively. Also 83.34% (n=50) cases showed F-wave abnormality.

Figure-3: CRP level and Results of Motor NCS (Median nerve) in patients with GBS

Figure-4: CRP level and Results of Motor NCS (CPN) in patients with GBS

In this study when we corelated the sensory nerve conduction study with CRP level, we observed that the result of sensory nerve conduction abnormalities in median nerve was positively associated with raised CRP level as shown in figure-5. However the sural nerve conduction study was negatively associated with raised CRP level as shown in figure-6. Sural sparing was observed in 70% (n= 42) cases.

Figure-5: CRP level and Results of Sensory NCS (median nerve) in patients with GBS

Figure-6

CRP level and Results Of Sensory NCS (sural nerve) in patients with GBS

Corelation study as also done between the ESR  level and result of nerve conduction study as shown in figure-7 and figure-8.

Results Of Motor and Sensory NCS

DISCUSSION:

Guillain-Barre syndrome is a severe autonomic disorder in which the immune system forms autoantibodies against healthy nerve cells of the peripheral nervous system and can be clinically diagnosed. Although exact cause is not known, it is triggered by many infectious illness like respiratory tract infection and gastroenteritis. [10] Nerve conduction study can help to diagnose and discriminate between axonal and demyelinating subtypes that could relate to prognosis. [11] C-reactive protein is one of the acute phase protein, the level of which rises in response to a number of nonspecific wide variety of disease including autoimmune diseases.[12]

In the present study, the mean age (yrs)of the GBS patients was 32.55(± 7.96) years. Similar type of result was reported by Mohamed et al, 2016 i.e. mean age was 38.74yrs.[13] But another previous study has reported higher mean of the GBS patients i.e. 43.7 years.[14]

Regarding sex distribution, we found GBS was more frequent among male (41) than the female (n=19). This result was in accordance with the result of a previous study by Dhadke et al, 2013 who reported 5.3% male and 41.77% female .[15]But another previous study reported no gender difference among GBS patients .[14]

Concerning triggering infection in GBS patients,  56.6% of patients were suffering from upper respiratory tract infection. This data was in agreement with results obtained by Willson et al., 2005 who reported 62.5% cases were history of URTI. [16] Another study by Newswagner et al.,2004 reported that most common preceding infection in 47.25% cases was Campylobacter jejuni. [17]. Another previous study in the year 2015, has reported that the most common antecedent events associated with GBS was gastrointestinal infection.[18]

Regarding CRP and ESR level in GBS patients in relation to disease severity, we found significantly raised level of both inflammatory markers in grade 4 and grade 5 patients also positive association between the CRP level as well as the ESR level in grade 4 and 5 GBS patients. Similar type of result was reported by a previous study by Vaishnavi et al in 2014 i.e 24.4% cases had raised ESR AND CRP level with bad prognosis.[3]

Patients of Guillain- Barre syndrome differ from each other regarding the degree as well as involvement of the motor and sensory nerves. The nerve conduction study result in majority of our patients (91.4%) shows decreased conduction velocity, decreased CMAP AND SNAP and  F- wave abnormalities (83.34%). Parmer et al study in 2013 also reported F-wave abnormalities in 90% case, prolonged distal latency in 0% cases, delayed conduction(73%) and abnormal SNAP(28%).[19] Our result is in agreement with the findings of a previous study conducted in the year 2012.[20]

CONCLUSION: -

The findings of this study suggest that inflammatory markers such as CRP and ESR, along with motor and sensory nerve conduction responses, are significantly associated with the clinical severity of Guillain–Barré Syndrome. Therefore, these parameters may serve as useful diagnostic as well as prognostic biomarkers in assessing disease severity and progression. The results may help clinicians in early risk assessment and in making timely therapeutic decisions, which could ultimately improve patient management and clinical outcomes.

However, despite the strengths of this study, it has certain limitations. As this was a cross-sectional study, causal relationships could not be established. Additionally, no attempt was made to differentiate between axonal and demyelinating subtypes of Guillain–Barré Syndrome, which may influence disease severity and prognosis. The ultimate outcome of this research is to provide supportive evidence that combining inflammatory markers with nerve conduction study findings can aid in better evaluation of disease severity and may contribute to improved prognostic assessment in patients with Guillain–Barré Syndrome.

REFERENCES:

1. Willison HJ, Jacobs BC, van Doorn PA. Guillain-Barre´ syndrome. Lancet 2016;388(10045):717Y727. doi:10.1016/ S0140-6736(16)00339-1.
2. Esposito S, Longo MR. Guillain-Barre´ syndrome. Autoimmune Rev 2017;16(1): 96Y101. doi:10.1016/j.autrev.2016.09.022.
3. Guillain-Barré Syndrome: Indications for Plasma Exchange. Transfusion Science, 1999; 20: 53–61.
4. Vaishnavi C, Kapoor P, Behura C, Singh SK, Prabhakar S. C-reactive protein in patients with Guillain Barre syndrome. Indian J Path Microbiol. 2014;57(1):51–4
5. Albers, J. W. & Kelly, J. J. Jr. Acquired inflammatory demyelinating polyneuropathies: clinical and electrodiagnostic features. Muscle Nerve 12, 435–51 (1989).
6. Gordon, P. H. & Wilbourn, A. J. Early electrodiagnostic findings in Guillain-Barre syndrome. Arch Neurol 58, 913–7 (2001).
7. Al-Shekhlee, A., Hachwi, R. N., Preston, D. C. & Katirji, B. New criteria for early electrodiagnosis of acute inflammatory demyelinating polyneuropathy. Muscle Nerve 32, 66–72 (2005).
8. Asbury AK, Cornblath DR. Assessment of current diagnostic criteria for GuillainBarré syndrome. Ann Neurol. 1990;27:21–4
9. Hughes RA, Rees JH. Clinical and epidemiologic features of Guillain-Barré syndrome. J Infect Dis. 1997;176(2):92–9.
10. Yuki N, Hartung HP. Guillain-Barré syndrome. N Engl J Med. 2012;366:2294–5.
11. Chiò A, Cocito D, Leone M, Giordana MT, Mora G, Mutani R. Guillain–Barré syndrome: a prospective, population based incidence and outcome survey. Neurology. 2003;60:1146–50.
12. Lau DC, Dhillon B, Yan H, Szmitko PE, Verma S. Adipokines. Molecular links between obesity and atherosclerosis. Am J Physiol Heart Circ Physiol. 2005;288:2031–41.
13. Mohamed NM, Magzoub MSM, Osman AA, Abdalla NM. Clinical and epidemiological study on inflammatory polyneuropathy (Guillain-Barré syndrome) among Sudanese cases. Int J Clin Med Res. 2016;3(1)
14. González-Suárez I, Sanz-Gallego I, Arpa J. Guillain-Barré syndrome: natural history and prognostic factors: a retrospective review of 106 cases. BMC Neurol. 2013;13:95.
15. Dhadke SV, Dhadke VN, Bangar SS, Korade MB. Clinical profile of Guillain Barre syndrome. J Assoc Physicians India. 2013;61:168–72
16. Willison HJ. The immunobiology of Guillain–Barré syndromes. J Peripher Nerv Syst. 2005;10:94–112
17. Newswanger DL, Warren CR. Guillain Barré syndrome. Am Fam Physician. 2004;69(10):2405–10.
18. Sudulagunta SR, Sodalagunta MB, Sepehrar M, Khorram H, Raja SKB, Kothandapani S, Noroozpour Z, Sham MA, Prasad N, Sunny SP, Mohammed MD, Gangadharappa R, Sudarshan RN. Guillain –Barré syndrome: clinical profile and management. GMS. 2015;13:1612–3174
19. Parmar LD, Doshi V, Singh SK. Nerve conduction studies in Guillian Barré syndrome. Int J Neurol. 2013;16(1):1–14
20. Rajabally YA, Uncini A. Outcome and its predictors in Guillain-Barre syndrome. J Neurol Neurosurg Psychiatry. 2012;83:711–8