Hyperventilation Syndrome, Treatment With L-Tryptophan and Pyridoxine; Predictive Values of Xanthurenic Acid Excretion

A case is made for the pathophysiological importance of the cerebral serotonergic neurons in the hyperventilation syndrome (HVS). Their function depends on the systemic L-tryptophan metabolism. The role of L-tryptophan metabolism is studied in 13 HVS patients, by administration of pyridoxine 125 mg t.i.d. and L-tryptophan two grams for four weeks. The xanthurenic acid excretion (XA) is measured as an index of the peripheral L-tryptophan metabolism, before treatment. The treatment resulted in freedom of hyperventilation attacks in nine patients. The XA was elevated or low in eight and normal in one of the nine responders and normal in the four non-responders. The extremes in the XA excretion had disappeared after treatment. Treatment results and XA data indicate that the L-tryptophan metabolism is important in the pathophysiology of the HVS, and that the XA discriminates responders from non-responders to pyridoxine, L-tryptophan treatment. 1 Lecturer for Biological Psychiatry, University of Nijmegen, The Netherlands; Dept. of Psychiatry, Bethesda Hospital, Tiel, The Netherlands. 2 Psychologist, Dept. of Social Psychiatry, University of Nijmegen. 3 Dept of Physiology, University of Nijmegen. Introduction The hyperventilation syndrome (HVS) is a functional syndrome (van Dis, 1978) caused by stress (Hermann et al., 1978). Important features of the HVS are the increased respiration, the anxiety, and an often occipitocervical headache and muscular hypertonia (Hardonk and Beumer, 1979; van Dis, 1978). The cerebral serotonergic neurotransmission (CST) is important to these symptoms on the basis of the following evidence from animal experiments: CST activates the inhibition of respiration that is found during an acute alcohol intoxication (Smith et al., 1975) or during Slow-Wave-Sleep (Jouvet, 1972). Animals depleted of serotonin have been used as experimental models of anxiety (Ellison, 1975). CST is important in the inhibition of pain (DeSousa and Wallace, 1977; Hoes, 1979-c). CST inhibits muscle tone as a result of an inhibition of afferent input (Hoes, 1979-c), a stimulation of Ren-shaw interneurons (MeyersLohman, 1971) and a suppression of monosynaptic reflexes (Clineschmidt and Andersen, 1970). Because of this evidence, underactivity of the CST is proposed as a pathophysiological model for HVS. As a matter of fact, the effectiveness of clomipramine in HVS was explained by its