As a part of the biochemical investigation of the changes accompanying the clinical cycle in periodic catatonia, the urinary excretion of catecholamines and their metabolites was studied longitudinally in one typical case of this illness. The patient has shown regularly repeated periods of catatonic stupor and remission for 18 yr. Chemical determination and clinical observations were carried out for 4 yr, covering 22 periods of stupor. Free norepinephrine (NE) epinephrine (E), and dopamine (DA) in 24-hr urine specimens were measured by fluorometric determination combined with thin-layer chromatography, and total normethanephrine (NMN), methanephrine (MN), vanillylmandelic acid (VMA), and homovanillic acid (HVA) were determined by paper chromatography. The patient was maintained on a vegetable free liquid diet during the periods of study. 1. 1. When not receiving drugs, the baseline levels of urinary catecholamine and metabolite excretion showed a remarkable increase in relation to the occurrence of catatonic stupors. E and MN reached their peak immediately after the onset of stupor and lasted for a short time, whereas NE and NMN reached their maximum values later and lasted during the whole stupor phase. This indicates that in this patient an acute psychotic upheavel reflects rapid stimulation of adrenals, whereas a prolonged stimulation of the sympathetic nervous system parallels the clinical course. In remission both E and NE and their metabolites returned to the lowest levels of excretion, similar to the levels in normal subjects. DA and HVA also showed parallel fluctuations with the clinical course but with less closer correlation. 2. 2. Treatment with 3 kinds of enzyme inhibitors involved in catecholamine metabolism, such as monoamine oxidase inhibitor, α-methyl-dopa, and disulfiram, altered the urinary excretion pattern of catecholamines and their metabolites with changes of clinical features. These trials gave us the impression that the patient might have no particular metabolic pathway disorder of catecholamines. 3. 3. Treatment with thyroid hormones, which proved themselves only to have slight benficial action on this case, resulted in a noticeable increase in catecholamines without consistent increase in their metabolites. 4. 4. Administration of reserpine not only had the striking effect on suppressing a relapse of stupor but also significantly suppressed the urinary excretion of NE, E, and their metabolites. The patient reacted on withdrawal of the drug with a recurrence of catatonic symptoms and rapid restoration of the biochemical parameters. 5. 5. Lithium citrate had no prophylactic effect on the relapse of the stupor, but only mitigated effects on the catatonic symptoms. Urinary excretion of E, NMN, and MN decreased inconsistently, but that of DA decreased consistently. These findings suggest that in the catatonic phase possibly the patient has an increased central noradrenergic activity, which may be associated with the clinical manifestations. However, the mechanism of overproduction or accumulation of NE in the central nervous system still remains obscure.