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Biomedical subjects

J M Rainey

Publications and source records attributed to J M Rainey.

At least 55 records · Page 3Linked to original sources
PubMed1984

Changes in the drug treatment of anxiety disorders.

One of the major changes in the clinical treatment of anxiety has been the substitution of benzodiazepines for less safe sedative-hypnotic drugs. A second major change has been the finding that antidepressants suppress panic attacks. The evidence for this is reviewed in this paper. It appears that panic anxiety is qualitatively different from other kinds of anxiety; this has important implications for diagnosis and treatment. Other clinical issues presented in this symposium are a review of benzodiazepine and new, non-benzodiazepine anxiolytic drugs, the treatment of separation anxiety, and the relationship of mitral valve prolapse to anxiety. Further advances are likely to depend both on our understanding of benzodiazepine and gamma-aminobutyric acid receptors and on drug models for inducing anxiety. The fact that antidepressants suppress panic attacks, and the ability to produce panic attacks in the laboratory opens up a number of possibilities for the investigation of the physiological basis of panic attacks. All of these topics are taken up in this symposium.

Agoraphobia↗
PubMed1984

Psychophysiological factors in panic disorder.

Panic disorder patients were compared with normal subjects during intravenous infusion of sodium lactate, isoproterenol, and placebo. Panic attacks meeting the criteria of the Diagnostic and Statistical Manual, vol. 3 [American Psychiatric Association, 1980] occurred during all three conditions in patients and during the lactate and isoproterenol infusions in normals. Patients had significantly higher average levels of skin conductance, heart rate and state anxiety, and significantly lower finger temperatures compared to normal subjects. However, no measure reliably differentiated panic attacks from nonattack periods. It is concluded that the peripheral physiologic responses investigated are neither necessary nor sufficient for the occurrence of panic attacks. It is possible that reports of these attacks represent phobic responses to intense anxiety.

Anxiety Disorders↗
PubMed1984

A comparison of lactate and isoproterenol anxiety states.

Both sodium lactate and isoproterenol can produce anxiety symptoms in patients with panic attacks. We administered both substances intravenously under placebo-controlled, double-blind conditions to patients with panic attacks and normal control subjects. We measured changes in anxiety levels using the Hamilton Anxiety Scale, State-Trait Anxiety Inventory, and a Panic Severity Scale. Measurements of respiratory rate and blood pH, pO2, pCO2, HCO3, and base excess were used to determine the relationship of hyperventilation to the symptoms induced by the infusions. Heart rate, epinephrine and norepinephrine levels were measured to determine whether there are changes related to palpitations and chest pain. Finger temperature and galvanic skin response were monitored to see whether any changes correlate with subject reports of hot or cold flashes and sweating. In this presentation, we will describe the clinical and biochemical changes that occur during panic attacks.

Adult↗
PubMed1982

The QT interval in drug-free depressed patients.

The QT interval is a noninvasive measurement obtained from electrocardiographic tracings. Long QT intervals occur in individuals at risk for fatal cardiac arrhythmias, and tricyclic antidepressant drugs can produce an increase in the QT interval. In this study, the authors compared the QT intervals from drug-free depressed patients, patients with substance use disorders, and normal control subjects. QT prolongation occurred more frequently (p less than .05) and severely (p less than .01) in the drug-free depressed subjects than in the controls. These results suggest that some drug-free depressed patients have increased QT intervals. These patients may be at risk for sudden, unexpected cardiac arrhythmias unrelated to the cardiotoxic effects of tricyclic antidepressant drugs.

Depressive Disorder↗
PubMed1982

Electrocardiographic changes following intravenous administration of thioridazine to macaque monkeys.

Treatment with thioridazine has been associated with electrocardiographic abnormalities, and there are individual case reports of fatal cardiac arrhythmias in patients taking thioridazine. Thioridazine or its metabolites can cause T-wave changes, but there is no evidence for a causal relationship between exposure to thioridazine and the occurrence of arrhythmias. In this study, the authors administered up to 6.7 mg/kg of thioridazine intravenously to macaque monkeys. Two of the animals had minimal T-wave changes immediately after the thioridazine injections and premature ventricular contractions a week later. The premature beats disappeared immediately after the next injection of thioridazine was administered. The authors suggest that when thioridazine has minimal effects on the T-wave, it may have both antiarrhythmic and arrhythmic activity. This could explain why cardiac arrhythmias have not been demonstrated in patients receiving regular, frequent doses of thioridazine, and suggests that arrhythmias may occur more frequently in patients with minimal T-wave changes.

Animals↗
PubMed1982

Tricyclic antidepressants and monoamine oxidase inhibitors in the treatment of agoraphobia.

The efficacy of tricyclic antidepressants and monoamine oxidase inhibitors for the treatment of agoraphobia and other panic disorders is reviewed with an emphasis on controlled prospective studies. After methodological biases are taken into account, there is strong evidence that antidepressants suppress panic attacks. This effect is not dependent on the presence of concomitant depressive symptoms. The clinical issues of dosage, delay in response, and relapse with discontinuation of treatment are also reviewed.

Agoraphobia↗
PubMed1979

Combination chemotherapy for advanced breast cancer utilizing vincristine, adriamycin, and cyclophosphamide (VAC).

Thirty-two patients with advanced breast cancer were treated with a combination of vincristine (1 mg/m2, not exceeding 2 mg, administered intravenously on day 1), adriamycin (40 mg/m2 administered intravenously on day 1), and cyclophosphamide (200 mg/m2 administered orally for 4 days on days 3-6). Courses were repeated at 21-28-day intervals. The mean age of the patients was 57 years (range, 30-79 years) and 18 patients were postmenopausal. None of the patients had received prior chemotherapy although 15 had prior endocrine treatment. Objective response was observed in 23 (72%) of the 32 patients and 9 responses (28%) were complete. The median remission duration was estimated to be 22 months. Median survival has not been reached but exceeds 24 months with a median time of follow-up of 17 months. Toxicity was acceptable and included mild nausea, vomiting, alopecia, and paresthesias. Only one instance of serious infection and no instances of bleeding were observed. The addition of vincristine to combination chemotherapy with adriamycin and cyclophosphamide appears to prolong the remission duration and survival in patients with advanced breast cancer to a greater extent than is achieved with adriamycin and cyclophosphamide alone.

Adult↗
PubMed1978

Safe, rapid administration schedule for cis-platinum-mannitol.

Cis-diamminedichloroplatinum (II) cis-plastinum, 25--75 mg/m2, with 40 gm mannitol and fluid were given over 1--2 hours to 40 patients with no evidence of elevated serum creatinine levels. Cis-plantinum was administered every 28 days at a dose of 50 mg/m2 to 22 patients, and 75mg/m2 to 6 patients. Patients received from one to eight courses of therapy with no change in their serum creatinine level. A safe, simple method of cis-platinum administration has been achieved.

Adult↗
PubMed1977

Disulfiram toxicity and carbon disulfide poisoning.

The author compared the neurotoxic effects of disulfiram with those of carbon disulfide, a disulfiram metabolite. The results suggest that carbon disulfide is responsible for the behavioral and neurological side effects of disulfiram. If this is so, then some other toxic effects of carbon disulfide, including parkinsonism, choreoathetosis, and thalamic syndrome may follow the ingestion of more than 5 g of disulfiram by adults, and individuals receiving as little as 125 mg of disulfiram per day may be at a three- to four-fold greater risk for arteriosclerotic cardiovascular disease than a comparable population not receiving the drug.

Animals↗
PubMed1975

Prolonged psychosis attributed to phencyclidine: report of three cases.

After ingesting street drugs sold as "PCP," "THC," and "methadone," three young men developed schizophreniform psychoses, analgesia, anesthesia, and amnesia for the psychotic state. Except for their unusually long duration of 2 to 4 weeks, these reactions resembled phencyclidine psychoses. The authors are aware of other phencyclidine-related hospital admissions but could find no information on phencyclidine in recently published handbooks on drug abuse.

Adolescent↗