Biomedical subjects
Publications and source records attributed to G D Burrows.
Hypnosis has a role in medical practice as an adjunct to many therapies. A brief review of the history, theory, induction procedures, phenomena and practice of hypnosis is given. The use of hypnosis in the therapy of anxiety is illustrated by a report of a 44-year-old woman suffering from an aeroplane phobia.
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An assessment of the side effects of therapeutic doses of tricyclic anti-depressant drugs was attempted in 32 patients with depressive illness. The patients studied had no evidence of clinical heart disease or hypertension and were not receiving any other drugs. Moderate increase in heart rate and mild prolongation of atrioventricular conduction occurred. No significant effect on the corrected QT interval or blood pressure was found. There was no correlation between the increased heart rate, prolongation of the atrioventricular conduction time (PR interval) and plasma nortriptyline levels measured in 20 out of 32 patients.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A double blind comparative study of amitriptyline and a new reversible MAO A inhibitor R011-1163 was conducted in 25 depressed inpatients over 4 weeks. Response to treatment was assessed with the Hamilton depression rating scale, the Carroll depression self rating scale and the Visual analogue scale. Both drugs produced significant changes in depressive symptomatology (P less than 0.01, MANOVA) and there were no statistically significant differences between drugs (P greater than 0.05 MANOVA). Side effects were of mild to moderate severity with dry mouth the most commonly reported side effect of amitriptyline and vague, generalised headache in patients, treated with R011-1163.
Platelet serotonin uptake was measured in 45 patients (12 males, 33 females) with panic attacks and 21 controls (9 males, 12 females). Higher Vmax values were obtained in the patient group than in the controls (100.2 +/- 11.5 vs. 34.9 +/- 3.8 pmol/10(8) platelets/min; P less than 0.0005) while the affinity constant Km was not significantly different (2.28 +/- 0.3 vs. 1.71 +/- 0.18 microM). A value of Vmax in excess of 60 pmol/10(8) platelets/min was observed in 60% of patients and in only 5% of controls. The results point to a specific abnormality of platelet serotonin uptake in patients with panic attacks.
The nocturnal synthesis of the pineal hormone melatonin was examined from 8 p.m. to midnight in 11 patients with panic disorder and eight control subjects. Patient concentrations of melatonin were significantly lower than controls at 10 p.m. (P less than 0.05; Kruskal-Wallis one-way ANOVA) and midnight (P less than 0.01). At 9 p.m. and 11 p.m., patient concentrations were also lower than controls, but were not statistically significantly different (P = 0.09). From these data, it is postulated that some patients with panic disorder exhibit a generalised defect in sensitivity of beta-adrenergic receptors or of sympathetic transmission.
Immunoreactive plasma beta-endorphin level was assayed in 33 patients with major affective disorder and in 16 psychiatrically normal controls before and after dexamethasone (1 mg) administration at 23.00 h. There were 18 cortisol suppressors and 15 non-suppressors among the patient group. All controls suppressed cortisol. Plasma beta-endorphin before dexamethasone was significantly different between suppressors, non-suppressors and controls (P less than 0.05, ANOVA). Concentrations of beta-endorphin were 4.7 +/- 0.7, 3.1 +/- 0.3 and 2.8 +/- 0.3 pmol/l for non-suppressors, suppressors and controls respectively. Following dexamethasone, beta-endorphin concentrations were again significantly different between groups (P less than 0.005, ANOVA). Concentrations were 4.6 +/- 0.7, 2.3 +/- 0.2 and 1.6 +/- 0.2 pmol/l for non-suppressors, suppressors and controls respectively. The implications of these findings are discussed.
This study compared findings of a community group of women (n = 32), who claimed they did not require help for menstrual cycle complaints, with a patient group (n = 75) with confirmed premenstrual syndrome (PMS). Subjects completed a battery of psychological tests to identify personality characteristics, levels of depression, anxiety, stress and marital adjustment. Menstrual cycle symptoms were assessed with the Menstrual Distress Questionnaire (MDQ, Moos, 1985) during follicular (day 6-8) and premenstrual phases (day 26-28) of two adjusted cycles and with daily symptom ratings. Daily 24-h urines were collected for oestradiol and pregnanediol levels for one cycle. After prospective assessment, the non-clinical sample were differentiated into those with pronounced cyclical symptom changes (Hi-volunteers, n = 13) and others with minimal cyclical changes (Lo-volunteers, n = 19). The total non-clinical sample could be distinguished from the patient group on depression, stress, and self-esteem scores. The non-clinical subgroup with pronounced cyclical symptoms is proposed as an 'at-risk' group for future treatment seeking.
A kinetic analysis of platelet monoamine oxidase (MAO) was performed in 22 patients with panic disorder and 14 normal controls, using tyramine as a substrate. Patients and controls did not differ significantly for either Km or Vmax, when same sex contrasts were carried out. The results do not support some studies that have shown elevated MAO activity in patients with panic attacks. The reasons for the discrepancies between previous studies and the present one are explored.
Platelet serotonin uptake and 3H-imipramine binding were measured in eight patients with panic disorders and nine controls. The Vmax of serotonin uptake was significantly elevated in patients compared to controls (77 +/- 14 vs. 50 +/- 4 pmol/10(8) platelets/min; P less than 0.05) while Km values were not different (1.46 +/- 0.41 vs. 1.24 +/- 0.20 microM). 3H-Imipramine binding to ruptured platelet membranes was not significantly different between patients and controls for either Bmax (395 +/- 71 vs. 412 +/- 107 fmol/mg protein) or Kd (0.90 +/- 0.18 vs. 1.09 +/- 0.30 nM). The implications for a serotonergic dysfunction in panic disorders are discussed.
Secondary depressive symptomatology in 435 subjects with panic disorder and phobic avoidance was studied before and after alprazolam treatment. No subject who had a primary affective disorder was included. Calculation of Hamilton Depression Rating Scale factor scores revealed that the agitation/anxiety, sleep disturbance, and somatization factors accounted for approximately 75% of the HAM-D total score; these all showed significant improvement with alprazolam treatment. There were few differences in dimensions of depressive symptomatology between those subjects with and those without major depression; the main difference was in the overall intensity of the depression.