A controlled comparison of trimipramine and amitriptyline.

Depressed patients seen in a private psychiatric practice (N = 41) were randomly assigned to receive trimipramine or amitriptyline over a study period of at least 4 weeks. Patients in both groups showed significant improvement over time on measures of mood and depression, and on psychological scales. Only one variable, the global improvement rating, showed a significant overall between-groups difference, which favored amitriptyline treatment. This difference may reflect the presence of significantly less baseline symptomatology in the amitriptyline group. Trimipramine patients were more seriously ill on initial diagnosis and showed significantly more improvement at week 2 than amitriptyline patients and a trend toward fewer side effects. Thus, trimipramine may be useful for patients particularly sensitive to side effects in whom evidence of early response is important.

Anxiety and/or the depressive syndromes.

The relationship of anxiety to depression in a number of the depressive and neurotic syndromes (agitated depressive syndrome, affective hypochondriacal syndrome, depressed obsessive-compulsive syndrome, phobic and obsessive-compulsive syndrome, anxiety state, depressive neurotic syndrome) is far from clear. Are anxiety and depression entirely separate disorders which may co-exist in the same patient? Does anxiety give rise to the depression? Does depression give rise to the anxiety? Are anxiety and depression manifestations of a single underlying disorders, dysphoria? Therapeutic responsivity to specific drugs suggest: relief of anxiety may reveal an underlying depression; anxiety syndromes which fail to respond to anxiolytics may respond to antidepressants; short-term relief of depression may occur at times with anxiolytics. Proposed mechanisms of action of depression and anxiety also involve overlap of the elements and systems involved. The basic sensations of pain, anticipation, depression and euphoria alone or in combination are sufficient to account for the dysphoric feelings and emotions when these sensations are associated with specific mental content. These may be related in turn to biogenic amines, beta-endorphins, diazepam receptors and possibly cocaine receptors.

beta-Endorphin and naloxone in psychiatric patients: clinical and biological effects.

The authors conducted single- and double-blind studies of the responses of 7 chronic male schizophrenic patients to 10 mg of naloxone. BPRS ratings were made before and 6 hours after the injection; ACTH blood levels were determined before and 1 1/2 and 6 hours after injection. Statistically significant improvement of psychotic behavior occurred after 6 hours. The greatest improvement occurred in the patient who showed the most pronounced diurnal variation of ACTH levels, and there was no improvement in the patient who had no diurnal changes. Prolactin plasma levels following endorphin injections were apparently dose-dependent and peaked at approximately 30 minutes. The mean half-life of elimination of exogenous beta-endorphin was between 12 and 35 minutes. The authors theorize that positive and negative behavioral responses to naloxone depend--as possibly do many placebo responses in general--on the relative stress produced by experimental or therapeutic interventions.

Monoamine oxidase inhibitors: potential for drug abuse.

Both the amphetamines and MAO inhibitors share common clinical and pharmacological properties, namely, (i) to clinically induce euphoriant-stimulating type and psychotomimetic effects in certain individuals, and (ii) to increase, albeit by different mechanisms, the amount of functionally available neurotransmitter (catecholamines and indoleamines) at the receptor site. The present data now indicate that, like the amphetamines, the use of MAO inhibitors can be clinically associated with dependence-tolerance. Perhaps these clinical findings will converge with other clinical-biochemical data in helping to define the specific amine(s) responsible for not only the clinical effects of these drugs but also the etiopathogenesis of major psychiatric illnesses such as the affective disorders and schizophrenia.

An unusual adverse reaction to self-medication with prednisone: an irrational crime during a fugue-state.

During five years of self-medication with Prednisone, a forty-one-year old asthmatic businessman experienced periods of euphoria, psychomotor hyperactivity, and poor judgement; a period of depression and anxiety during temporary steroid withdrawal; and finally, with resumption of Prednisone, episodes of grandiosity and bizarre fugue-like behavior, with adoption of a second identity and culminating in an irrational crime. Steroids were then withdrawn, and the patient resumed his premorbid personality, but had amnesia for much of his previous behavior. The literature on hysterical fugues and corticosteroid-induced mental disturbance is reviewed. The patient's reactions are analyzed in terms of his premorbid neurotic conflicts, the psychological stresses acting upon him, and the effects of Prednisone on his central nervous system.

Studies on the mechanism of lithium action: preliminary report.

Preliminary observations in a small animal sample reveal that chronic lithium treatment in rats produced significant changes in the microvillous processes on the cell surface of the choroid plexus. These alterations may be associated with increased intracellular choroidal volume. The type of changes noted by SEM suggest an alteration in movement of water into the extracellular areas of the brain. This basic alteration produced by lithium in the secretory/absorptive capacity of the chorid plexus is probably reversible.