Search

Long-term treatment of rats with haloperidol produced an increased sensitivity to the locomotor and stereotypic effect of apomorphine. This behavioral dopaminergic supersensitivity was accompanied by increased binding of [3H] spiroperidol in the striatum. Rats treated concurrently with lithium and haloperidol failed to develop both behavioral sensitivity to apomorphine and increased striatal dopamine receptor binding. The ability of lighium to prevent recurrent manicdepressive episodes may be related, in part, to its ability to stabilize dopaminergic receptor sensitivity.

Fourteen schizophrenic patients and five patients with affective disorders were given naloxone (0.4 to 10 milligrams) or placebo intravenously in a double-blind fashion. Physicians' ratings of hallucinations, mannerisms and posturing, conceptual disorganization, psychosis, and mood did not change significantly. A single item, unusual thought content, improved significantly on the naloxone day compared to the placebo day. There was no improvement in mood in affectively ill patients rated either by themselves or by physicians. Naloxone did not markedly improve any patient studied, which suggests that the acute blockade of opiate receptors is not associated with global improvement in psychotic symptomatology.

Eight chronic schizophrenia patients completed a research program consisting of ten weekly sessions of active hemodialysis and ten weekly sessions of sham dialysis in a double-blind design. Previous reports of therapeutic efficacy were not substantiated. None of the patients improved during active dialysis; four patients worsened.

Marked elevations of urinary adenosine 3',5'-monophosphate occurred on the day of rapid switch from a depressed into a manic state in patients with manic-depressive illness. It is suggested that this increase might serve a trigger function for the process by which catecholamines are elevated during the manic phase of the illness.

Concentrations of the norepinephrine metabolite 3-methoxy-4-hydroxyphenyl glycol in cerebrospinal fluid were measured by a gas chromatographic method in 34 patients with affective illness and in 44 controls. Concentrations of this metabolite in spinal fluid were significantly lower in depressed patients than in controls or manic patients. These low values may occur secondary to depressive phenomena such as reduced psychomotor activity, or they may reflect a primary change in norepinephrine metabolism in depressive illness.