Ranan Rimon

Serum and CSF levels of haloperidol by radioimmunoassay and radioreceptor assay during high-dose therapy of resistant schizophrenic patients

Serum and cerebrospinal fluid (CSF) levels of haloperidol were measured in 12 chronic neuroleptic-non-responsive schizophrenic patients after 1 month on 60 mg haloperidol daily and then again after 1 month on 120 mg haloperidol daily. Serum haloperidol and CSF haloperidol rose with increasing dose. Serum and CSF levels were significantly correlated. No clinical improvement was achieved despite the high serum and CSF drug levels.

Cyclic GMP in the CSF of patients with schizophrenia before and after neuroleptic treatment

Cerebrospinal fluid (CSF) cyclic GMP may derive from central cholinergic neurotransmission. Measurement of CSF cyclic GMP may allow evaluation of possible implications of the dopaminergic hyperactivity in schizophrenia proposed by the dopamine hypothesis. The CSF cyclic GMP levels in 27 drug-free schizophrenic patients was measured and compared to that in 9 psychiatrically-healthy individuals. The mean CSF cyclic GMP level of the schizophrenic patients was 23% lower than that of the control group, but this difference, did not attain statistical significance. In addition the CSF cyclic GMP levels in a group of 10 schizophrenic patients were compared before and after 2 months of neuroleptic treatment. The mean level of cyclic GMP rose 50% after treatment with phenothiazines (P<0.05). These results could indicate some tendency for decreased activity of central cholinergic neurons in schizophrenia as well as a restored dopaminergic-cholinergic balance after neuroleptic treatment.

Neuroleptics Reduce Spinal Fluid Cyclic AMP in Schizophrenic Patients

Cyclic AMP in the cerebrospinal fluid (CSF) was determined in a group of 10 schizophrenic patients before neuroleptic drug treatment and after a mean of 8 weeks antipsychotic drug therapy. For 8 patients with marked to moderate treatment response a significant (p less than 0.01) decline in CSF cyclic AMP was observed. This result is consistent with the theory that blockade of postsynaptic dopamine receptors is a major mechanism of the antipsychotic action of neuroleptic drugs.

Electrophoresis of platelet monoamine oxidase in schizophrenia and manic-depressive illness.

Monoamine oxidase is an important enzyme in the catabolism of biogenic amines and can be measured in human platelets. Platelet MAO has been reported to be reduced in schizophrenic and manicdepressive patients, though other reports are contradictory. The present study evaluated the possibility that qualitative genetic enzyme abnormalities of MAO could be responsible for the different enzyme activities of platelet MAO in different populations. However, polyacrylamide gel electrophoresis of platelet MAO from 10 manic‐depressive, 12 schizophrenic, and 11 normal individuals did not reveal any genetic mutant forms.

Platelet Monoamine Oxidase in Women with Premenstrual Syndrome

Platelet monoamine oxidase (MAO) and RBC catechol-O-methyltransferase (COMT) were studied in 12 women suffering from premenstrual syndrome. No significant variation of platelet MAO or RBC COMT was found during the menstrual cycle, as opposed to previous studies on normal women and monkeys, which report a significant decline of platelet MAO activity in the 5-day period before menses.

The effect of haloperidol on epinephrine-stimulated adenylate cyclase in humans.

Administration of epinephrine in man has been shown previously to lead to a rise in plasma cyclic AMP levels by activation of the β-adrenergic-stimulated adenylate cyclase. Therapeutic doses of lithium in humans block the epinephrine-induced rise in plasma cyclic AMP levels, suggesting that lithium inhibits β-adrenergic adenylate cyclase. In contrast, ten subjects receiving haloperidol, a drug also effective in the treatment of mania, show a mean rise in plasma cyclic AMP levels after epinephrine administration and the magnitude of the response is the same as for non-drug treated individuals. These findings are discussed in relation to the possible pharmacological mechanisms of action of lithium and haloperidol in the control of mania.

Antibody Levels to Viruses in Psychiatric Illness

It has long been known that certain viruses are neurotropic and that they can cause encephalitis and post-encephalitic syndromes which can be confused with psychotic disorders (1,2). It has, however, only recently been shown that viruses may have incubation periods of twenty years or more before signs of central nervous system (CNS) disease appear. Such viral infections are referred to as slow or latent to indicate the time lag between the introduction of the virus into the host and the production of the clinical symptoms.