Predicting Respiratory Failure in Guillain-Barré Syndrome (GBS)

Abstract & Commentary

By Michael Rubin, MD, Professor of Clinical Neurology, Weill Medical College of Cornell University, NewYork-Presbyterian Hospital. Dr. Rubin is on the speaker's bureau for Athena Diagnostics, and does research for Pfizer and Merck.

Synopsis: Phrenic nerve conduction studies may be a promising method to anticipate respiratory failure in patients with GBS.

Source: Ito H, Ito H, Fujita K, et al. Phrenic nerve conduction in the early stage of Guillain-Barre syndrome might predict the respiratory failure. Acta Neurol Scand 2007; 116:255-258.

Predicting respiratory failure early in the course of Guillain-Barré syndrome (GBS) by a simple, accurate method would decrease morbidity and mortality. Blood gas measurements, forced vital capacity, negative inspiratory force, and clinical acumen are notoriously insensitive. Phrenic nerve conduction studies may prove helpful. Nerve conduction studies were performed on 15 patients admitted between 1999 and 2006 to the Kansai Medical University Department of Neurology (Osaka, Japan) with clinical and cerebrospinal fluid findings characteristic of GBS. None had received immunomodulating therapy, including intravenous immunoglobulin or plasma exchange, and none were ventilated or receiving oxygen. Phrenic nerve stimulation was performed percutaneously, posterior to the sternocleidomastoid muscle, at the upper level of the thyroid cartilage, with diaphragmatic recording on the anterior axillary line at the 8th intercostal space. Distal latency and peak-to-peak amplitude of both phrenic nerves were summed. Statistical analysis was performed using the Mann-Whitney non-parametric rank sum test, with P < 0.05 considered significant.

Three patients with summed phrenic nerve latency > 30 ms required ventilatory assistance, one by mechanical means and two with oxygenation. Bilateral diaphragmatic peak-to-peak amplitude was < 0.3 mV in these patients. None of the patients with summed latency < 30 ms required respiratory assistance, and all but one of these had a summed amplitude > 0.3 mV. Respiratory embarrassment was not found to correlate with the presence of bulbar palsy, anti-ganglioside antibodies, or the results of conventional peripheral nerve conduction studies, including the tibial, peroneal, median, or ulnar nerves. Vital capacity less than 80% was seen in only one patient with summed latency > 30 ms. Respiratory failure in GBS may be predicted by the presence of increased summed latency or motor amplitude of bilateral phrenic nerves. Larger studies are warranted to confirm this notion.


Among 154 patients with GBS seen between 1998 and 2006, the demyelinating, rather than the axonal, form of GBS was more predictive of the need for mechanical ventilation (p = 0.0003). Vital capacity greater than 81%, and an amplitude drop of less than 45.5% in distal to proximal peroneal nerve motor evoked response, was associated with less than a 2.5% likelihood of requiring ventilation.1 Clinical and electrophysiological parameters can be useful predictors of respiratory failure in GBS. None is fail safe, but thorough investigation of such patients should forestall the unexpected.


1. Durand MC, et al. Lancet Neurol 2006; 5:1021-1028.