Dysautonomia in Guillain-Barre syndrome

About 20% of all GBS patients have symptoms of dysautonomia:labile hypertension, orthostatic hypotension, sinustachycardia or sinus arrest. This rate rises to 75% in patients with tetraplegia. Proprioceptive loss predicts dysautonomia independently from the severity of weakness. It is frequently responsible for dysautonomia. The afferent limb of cardiovascular regulation contains more myelinated fibers than the sympathetic and parasympathetic efferences, which determine the common classification of dysautonomia. The frequence of mixed sympathetic and parasympathetic hyperactivity is hard to explain by efferent lesions. Afferent conduction block releases the sympathetic efference of the baroreceptor reflex. The resulting catecholamine excess explains hypertension, tachycardia, EGG-changes and hyperglycemia. Norepinephrine sensitizes left ventricular stretch receptors. They induce cardiovascular depression and neurocardiogenic syncope which has a temporal behaviour similar to the blood pressure variations of GBS. Conduction block of sinoatrial stretch receptors causes inappropriate secretion of ADH and renin. Disbalance between myelinated and unmyelinated afferents which decrease and increase heart rate may cause parasympathetic hyperactivity, as exemplified by pulmonary stretch receptors that are stimulated by artificial ventilation. Wrong afferent feedback is responsible for many cardiovascular instabilities in GBS. Blockade of misguided efferent reactions is an attractive therapeutical approach.