The effect of propranolol on CSF amine metabolites in psychiatric patients.

Abstract

In view of the central side effects of beta‐adrenoceptor blocking agents and their alleged antipsychotic action in the absence of DA receptor blockade, it is important to establish which neurotransmitters are likely to be involved. Previous animal and patient studies have, however, produced conflicting data on this point. The changes in CSF HVA, 5HIAA and MHPG during treatment with propranolol (960 mg/day) in chronic schizophrenic patients were monitored on four occasions over 30 days. Clinical changes were monitored by the Wing and Krawiecka Scales and motor activity was assessed by pedometer. CSF HVA levels were significantly increased by propranolol and the rise continued throughout the 30 day period. There were no significant changes in the other metabolites. There was no evidence of any therapeutic benefit from propranolol treatment in these patients. These findings may explain the central side‐effects and occasional reports of schizophreniform psychosis after propranolol, since an increase in DA turnover occurs without DA receptor blockade.

Hypothalamic Antihypertensive Effect of Metoprolol in Chronic Aortic Coarctated Rats

“…found that large doses of propranolol induced increases in 5‐HIAA and MHPG levels in the cerebrospinal fluid without changing DOPAC levels. However, in another report, 18 propranolol increased homovanillic acid levels in psychiatric patients without affecting levels of HIAA and MHPG. Tuross and Patrick 10 found that propranolol produced an inhibition of tyrosine hydroxylase activity with a reduction of dopamine formation.…”

One More Look at Propranolol for the Treatment of Refractory Schizophrenia

“…Among those negative studies of the effect of propranolol alone in neuroleptic-refractory schizophrenia, the study by Gardos et al (1973) with an n of 8 at best could attain a power level < .31; the study of King et al (1983) of 12 patients could reach a power level of .46; and the study of Peet et al (1981) of 53 patients in three sample groups—believed by some to be a strong refutation of earlier positive findings—reaches a power of .73 only if the true effect were a large one. Were there, in fact, a medium-sized effect to be detected, the study of Peet et al would have a power of only .34.…”