ISPUB.COM The Internet Journal of Neurology Volume 16 Number 1 1 of 14 Nerve Conduction Studies In Guillian Barre’ Syndrome L D Parmar,, V Doshi, S K Singh Citation L D Parmar,, V Doshi, S K Singh. Nerve Conduction Studies In Guillian Barre’ Syndrome . The Internet Journal of Neurology. 2013 Volume 16 Number 1. Abstract BACKGROUND: NCS are objective methods for diagnosis, quantification and classification of poly neuropathies. Electrophysiology is most important to confirm GBS in all its forms. Aim: To study early characteristics of NCS in GBS. Research design: Cross sectional, analytical Material & Methods: NCS performed on 49 GBS participants were retrospectively analyzed. Different parameters motor, sensory, late waves studied & compared with literature. Statistics: Descriptive statistics, ANOVA, correlations. Results: Age range 1-82 yrs. 76% males, AIDP form (93.88%) predominates, CMAP median bilaterally moderately associated with muscle grades p value 0.005 & 0.006, CMAP & F disturbance severe and predominant feature. 41.86 % H- reflex un recordable. 34.69% showed sensory abnormalities. Age group ≤ 3 years showed similar pattern. 3 children showed in excitability. Abnormality in number of variables of nerves in combination is likely pattern. Conclusions: Early NCS pattern emerged similar to several studies. INTRODUCTION Polio has been eradicated in most parts of the world and presently Guillain-Barré syndrome (GBS) is the most common cause of acute flaccid paralysis, severe generalized paralysis1, 2, 3,4,5,6, 8, 17, 30 Guillain-Barré syndrome (GBS), or better Guillain-Barré-Strohl syndrome to recognize the three authors responsible for the first description of this disorder. Georges Guillian, Jean Alexander Barre’ and Andre’ Strohl in 1916 related a benign acute poly¬neuritis in three soldiers, with increase in protein levels without pleocyto¬sis (albumin-cytological dissociation).9, 10, 11, 12 The annual incidence of GBS has been reported to be relatively uniform between 0.4 and 4 cases per 100000 per year throughout the world.1, 3, 4, 5, 7, 12, 14, 15, 22, 24, 29, 30, 31 But the most recent and careful population based studies report an incidence of 1.2 – 1.9 per 100000 4, 13, 15, 20, 27, 28, 29. The lifetime likelihood of any individual acquiring GBS is 1:1000. It is now appreciated that GBS is not a single disorder but again a syndrome of several types of acute immune- mediated polyneuropathies. The most commonly proposed mechanism for the development of autoimmune disease is molecular mimicry (Yuki, 2005). Molecular mimicry refers to the situation where the pathogen and host share nearly identical antigens, which induces an antibody and T cell immune response that is cross reactive.5,7,8,10,11,12,13,14,15,19,22,23,27,28. The onset of symptoms can either be acute or sub acute. Gradual recovery takes place after a plateau phase. The disease usually progresses over 2-4 weeks.5 The condition reaches its nadir by 2 weeks in most cases and in 4 weeks in nearly all.15, 18, 22 Current diagnostic criteria include <4 weeks of progression to clinical nadir7, 47 Electrophysiology represents the most important laboratory study to confirm the diagnosis of GBS in all its forms. 5, 10, 11, 13, 15, 19, 21, 22, 25, 32, 33, 34, 35, 36, 37, 38,39,40,41,42,43,44 Electrophysiological testing must be done as early as possible after presentation and should be repeated on a weekly basis to further confirm diagnosis and for prognostic purposes13. Another important aspect of studying the nerves early is that it provides the best chance to allow differentiation between demyelinating and axonal forms of GBS. In severe cases of demyelinating GBS, axonal loss will occur over time and, as it does, nerves become inexcitable. Presence of early motor nerve inexcitability represents a reliable marker of axonal polyradiculoneuropathy.13