Dysautonomia in Guillain-Barre syndrome

About 20% of all GBS patients have symptoms of dysautonomia:labile hyperten sion, orthostatic hypotension, sinustachycardia or sinus arrest. This rate rises to 75% in patients with tetraplegia. Proprioceptive loss predicts dys autonomia independently from the severity of weakness. It is frequently res ponsible for dysautonomia. The afferent limb of cardiovascular regulation c ontains more myelinated fibers than the sympathetic and parasympathetic eff erences, which determine the common classification of dysautonomia. The fre quence of mixed sympathetic and parasympathetic hyperactivity is hard to ex plain by efferent lesions. Afferent conduction block releases the sympathet ic efference of the baroreceptor reflex. The resulting catecholamine excess explains hypertension, tachycardia, EGG-changes and hyperglycemia. Norepin ephrine sensitizes left ventricular stretch receptors. They induce cardiova scular depression and neurocardiogenic syncope which has a temporal behavio ur similar to the blood pressure variations of GBS. Conduction block of sin oatrial 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 exemplifie d by pulmonary stretch receptors that are stimulated by artificial ventilat ion. Wrong afferent feedback is responsible for many cardiovascular instabi lities in GBS. Blockade of misguided efferent reactions is an attractive th erapeutical approach.