No abstract

Xanthurenic acid is a metabolite of L-tryptophanicotinic acid ribonucleotide biosynthesis. The excretion of xanthurenic acid from urine 24 h after ingestion of 5 g L-tryptophan is increased in depressive patients, and 17-hydroxycorticosteroids are considered of primary importance to this disorder. However, in this study, the excretion of xanthurenic acid and 17-hydroxycorticosteroids did not correlate with the scores of the Raskin depression scale, Hamilton depression scale, Zung depression scale, or the Zung anxiety scale in depressive patients. The patients were treated with either pyridoxine plus L-tryptophan, a presumably serotonin-enhancing treatment (n = 10) or maprotiline, a noradrenaline-enhancing drug (n = 10). Repeated measurements showed no differences between treatments after 2 or 4 weeks of treatment. The improvement in xanthurenic acid excretion precedes clinical improvements in depression. The excretion of xanthurenic acid only at 2 weeks correlated significantly with the anxiety and depression scores at 4 weeks, making prediction of clinical improvement possible. The neurobiological mode of action on noradrenergic or serotonergic neurons of antidepressant medication is of questionable significance to their therapeutic effect.

No abstract

The Tolosa-Hunt syndrome is a superior orbital fissure and/or anterior cavernous sinus syndrome. Because the etiology is unknown, the differential diagnosis is essentially one of localization. The pathological substrate consists of a non-specific inflammation. An exhaustive literature search up to 1 January 1981 yielded altogether 214 cases. Seven personal cases are reported. A consistent pathogenesis still lacking. Observations made in four cases led to the hypothesis that the syndrome results from dysregulation of the adaptation to stressful events, involving enhanced serotonergic activity which suppresses ACTH secretion and promotes non-specific inflammation of perivascular (venous/arterial) tissue.

Six patients suffered from a hyperventilation syndrome for 3.4 +/- 1.2 years. They had a lowered PAco2 at rest and an abnormal CO2 response curve. During the entire period they had received unsuccessful treatment with anxiolytics, and had also undergone behaviour therapy for the last 1 -- 2 years without success. Both treatments were discontinued and the patients were placed on clomipramine, 25 mg t.i.d. for 9 months. Their anxiety and hyperventilation attacks diminished after one month of clomipramine, and their fear of attacks an their phobias subsided after two months. Eighteen months after clomipramine therapy had been initiated, they were feeling well without medication. The possible mode of action of clomipramine on the hyperventilation syndrome via central serotonergic mechanism is discussed.