[A study of parasympathetic functions in Guillain-Barré syndrome]

Sympathetic hyperactivity in Guillain-Barré syndrome (GBS) may be due to the involvement of afferent fibers in the vagus and glossopharyngeal nerves within the baroreceptor pathway. Patients with GBS who have increased sympathetic nervous activity, do not, however, always show baroreceptor dysfunction such as orthosatic hypotension. We evaluated parasympathetic nervous activity in patients with GBS to clarity the mechanism of autonomic deficits. An atropine test (20 micrograms/kg intravenous bolus infusion) and hemodynamic functional tests were conducted on 6 patients with GBS (49.5 +/- 13.6 years old) and age-matched healthy controls; 11 controls (50.5 +/- 17.6 YO) for atropine test and 81 controls (48.5 +/- 8.8 years old) for hemodynamic functional tests. I. Parasympathetic nervous activity: (a) Atropine test: (1) Increase in pulse rate after the administration of atropine; the degree was significantly higher in the patients with GBS than that in the healthy controls (p = 0.027). (2) Atropine ratio (= increase in pulse rate following intravenous administration of atropine)/(mean pulse rate before the administration); the ratio was significantly higher in the patients with GBS than that in the healthy controls (p = 0.026). (b) Aschner eyeball pressure test: The degree of reflex bradycardia in the patients with GBS was significantly higher that the in the healthy controls (p = 0.039) II. Sympathetic nervous activity: (a) Cold pressor test: The degree of reflex hypertension was significantly higher in the patients with GBS than in the healthy controls (p = 0.008). (b) 70 degrees passive head-up test: Falls in systolic and diastolic blood pressure in the patients with GBS tended to be lower than in the healthy controls (p = 0.092, p = 0.091). These results suggest that both parasympathetic and sympathetic nervous activities increased, and the baroreceptor function is well preserved in GBS. We thus surmise that increased sympathetic nervous activity in GBS is not explained by reduced inhibition of the parasympathetic nervous activity.