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COMMENTARY
Year : 2016  |  Volume : 64  |  Issue : 5  |  Page : 921-922

Electrophysiological features of Gullian Barre syndrome: Newer insights


Department of Neurology, Janakpuri Super Speciality Hospital, New Delhi, India

Date of Web Publication12-Sep-2016

Correspondence Address:
Man Mohan Mehndiratta
Department of Neurology, Janakpuri Super Speciality Hospital, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.190277

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How to cite this article:
Mehndiratta MM, Wadhwa A. Electrophysiological features of Gullian Barre syndrome: Newer insights. Neurol India 2016;64:921-2

How to cite this URL:
Mehndiratta MM, Wadhwa A. Electrophysiological features of Gullian Barre syndrome: Newer insights. Neurol India [serial online] 2016 [cited 2019 Sep 23];64:921-2. Available from: http://www.neurologyindia.com/text.asp?2016/64/5/921/190277




Gullian Barre syndrome (GBS) is classically a clinical diagnosis but electrophysiology and nerve conduction studies (NCS) help in supporting the diagnosis, making a distinction between axonal and demyelinating variants as well as helping in prognostication. The characteristic findings supportive of acute inflammatory demyelinating polyradiculoneuropathy include prolonged distal motor latencies, reduced conduction velocities, conduction blocks at non-entrapment sites, temporal dispersion and prolonged F wave latencies.

The article on “Electrophysiological observations in critically ill Guillain–Barre syndrome” in this issue by Nagappa et al.,[1] further highlights the importance of electrophysiological abnormalities and its role in predicting duration of mechanical ventilation in this group of patients. The role played by critical illness polyneuropathy, the syndrome of acute weakness affecting limb and respiratory muscles on prolonged stay in the intensive care unit, as a contributor in delayed recovery and as an electrophysiological confounder in patients of severe GBS needs to be taken into account.

Gullian Barre syndrome (GBS) has been classically described as an acute inflammatory demyelinating polyradiculoneuropathy (AIDP). However, an increasing number of variants and subtypes have been recognized over the past few decades. The rubric term “Gullian Barre syndrome” also includes axonal and the more restricted variants like Miller Fisher syndrome, which is characterized by a triad of ataxia, ophthalmoplegia and areflexia. Other variants include the so-called pharyngeal-brachial variant, which is characterized by pharyngeal and cervicobrachial weakness; and, the paraparetic variant, in which the weakness is limited to the lower limbs and later progresses to involve the arms.

In 1859, Landry first described the clinical features of GBS.[2] Gullian, Barre and Strohl subsequently in 1916 suggested the characteristic cerebrospinal fluid (CSF) examination findings of albumin-cytological dissociation in two French soldiers. The role of plasma exchange and intravenous immunoglobulins as efficient treatment modalities was established in the 1980s and 1990s, respectively.[3],[4]

The abnormalities in NCS may be recorded by the end of first week of illness and are most pronounced by the second week after the onset of weakness. To increase the certainty of diagnosis with NCS and to increase the diagnostic yield, recordings at least four motor nerves, three sensory nerves, F waves and H- reflexes should be obtained.[5]

The characteristic findings supportive of acute inflammatory demyelinating polyradiculoneuropathy include prolonged distal motor latencies, reduced conduction velocities, conduction blocks at non-entrapment sites, temporal dispersion and prolonged F wave latencies. Another valuable electrophysiological characteristic of GBS is “sural sparing” that denotes a normal sural sensory nerve action potential with abnormal upper extremity sensory nerve responses.[6] This pattern is very unlikely for neuropathies other than AIDP. Sural sparing, persists even the later part of the disease as. Similarly, a high i.e., greater than one, sensory ratio (sural + radial sensory nerve action potentials (SNAPs)/median + ulnar SNAPs) is quite helpful in distinguishing GBS from other polyneuropathies.[7] Another role played by NCS in GBS is in prognostication and in assessing the need and duration of ventilatory support in patients presenting with a severe disease. Low compound muscle action potentials (CMAPs) are most predictive of a poor prognosis.[5]

The article on “Electrophysiological observations in critically ill Guillain–Barre syndrome” in this issue by Nagappa et al., further highlights the importance of electrophysiological abnormalities and its role in predicting the duration of mechanical ventilation in this group of patients.[1] The authors have emphasized that reduced amplitude or absent motor potentials correlate with requirement for longer duration of ventilation. In this article, unexcitable sensory nerves were more common in patients who could be weaned off ventilator within 15 days and there was no relation between the conduction blocks in motor nerves and the duration of ventilation. It is well known that a longer duration of mechanical ventilation and reduced amplitude of motor CMAP increases the morbidity and a poor outcome. But this study stresses certain associations, such as abnormalities in motor nerves are more frequent in patients requiring prolonged mechanical ventilation, while sensory nerve abnormalities are commoner in patients who recover within two weeks. These associations may add to objective prognostication.

The role played by critical illness polyneuropathy, the syndrome of acute weakness affecting limb and respiratory muscles on prolonged stay in the intensive care unit, as a contributor in delayed recovery and as an electrophysiological confounder, in patients suffering from severe GBS and on mechanical ventilation, needs to be taken into account.[8] It affects male and female subjects of all age groups being relatively less common in children. It presents as generalized flaccid weakness with less frequent affliction of cranial nerves. Nerve conduction studies are more consistent with findings of distal axonal polyneuropathy with decreased compound muscle action potential (CMAP) and less commonly, sensory nerve action potential (SNAP) amplitudes. Also, needle electromyography shows fibrillation potentials and decreased motor unit action potentials. The cerebrospinal fluid study is almost always normal, helping in its differentiation from GBS.

Further studies in this regard are required to determine appropriate prognostication markers and electrophysiological parameters for assessing the occurence of an early respiratory failure and for estimating the duration of mechanical ventilation in critically ill GBS patients. Furthermore, the finding from the study of Nagappa et al., that patients with unexcitable sensory nerves require shorter mechanical ventilation needs to be reproduced in other studies before it may be taken as a definitive marker.[1]

 
 » References Top

1.
Nagappa M, Netto AB, Taly AB, Kulkarni GB, Umamaheshwara Rao GS, Periyavan S, Rao S. Electrophysiological observations in critically ill Guillain–Barre syndrome. Neurol India 2016;64:914-20.  Back to cited text no. 1
[PUBMED]  Medknow Journal  
2.
Prineas JW. Pathology of the Guillain-Barre´ syndrome. Ann Neurol 1981;9(suppl):6-19.  Back to cited text no. 2
[PUBMED]    
3.
French Cooperative Group on Plasma Exchange in Guillain-Barre´ Syndrome. Efficiency of plasma exchange in Guillain-Barre´ syndrome: Role of replacement fluids. Ann Neurol 1987;22:753-761  Back to cited text no. 3
    
4.
Plasma Exchange/Sandoglobulin Guillain-Barre´ Syndrome Trial Group. Randomised trial of plasma exchange, intravenous immunoglobulin, and combined treatments in Guillain-Barre´ syndrome. Lancet 1997;349:225-30  Back to cited text no. 4
    
5.
Willison HJ, Jacobs BC, van Doorn PA. Guillain-Barré syndrome. Lancet 2016 Feb 29. pii: S0140-6736(16) 00339-1.  Back to cited text no. 5
    
6.
Gordon PH, Wilbourn AJ. Early electrodiagnostic findings in Guillain–Barré syndrome. Arch Neurol 2001;58:913-7.  Back to cited text no. 6
[PUBMED]    
7.
Al-Shekhlee, A, Hachwi, RN, Preston DC, Katirji B. New criteria for early electrodiagnosis of acute inflammatory demyelinating polyneuropathy. Muscle Nerve 2005;32: 66-72.  Back to cited text no. 7
    
8.
Ramrakhiani N. Stuck to the ventilator: The neuromyopathy of critical illness. Neurol India 2016;64:604-5.  Back to cited text no. 8
[PUBMED]  Medknow Journal  




 

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