Biomedical subjects

R J Maddock

Publications and source records attributed to R J Maddock.

At least 19 recordsLinked to original sources

PubMed1996

An effect of alcohol on the distribution of spatial attention.

OBJECTIVE: Previous research on the effects of alcohol on visual performance led us to the prediction that alcohol should interfere with the distribution of visual spatial attention. This prediction was examined in two experiments that measured the effect of alcohol on reaction time (RT) for tasks that differed in visual spatial attention requirements. METHOD: In the first experiment, 48 adult volunteers (33 female) responded to either the onset or offset of one of five potential targets without alcohol to determine the relative demands on attention of stimulus onset and offset. The spatial extent of the five-target display was also varied. In the second experiment, the effect of alcohol was determined for both the onset and the offset tasks in 12 adult volunteers (nine female). RESULTS: The offset task was found to place greater demands on spatial attention as the increase in display area result in relatively greater increases in RT. Alcohol increased RT in the offset task for the larger, but not the smaller, display, and there were no significant effects of alcohol for the onset task. CONCLUSIONS: The results indicate that alcohol impairs performance on tasks that place greater demands on visual spatial attention and likely disrupts the ability to shift attention from one spatial locus to another during serial search.

Adolescent↗

PubMed1995

Adinazolam-SR in panic disorder with agoraphobia: relationship of daily dose to efficacy.

BACKGROUND: We report the results from a multicenter, double-blind, randomized, fixed-dose study designed to evaluate the relationship between daily dose and efficacy of adinazolam-SR in patients with panic disorder with agoraphobia. METHOD: Patients (N = 315) were randomized to one of four treatment groups (placebo, N = 83; 30-mg group, N = 79; 60-mg group, N = 81; and 90-mg group, N = 72) and then treated twice daily for 4 weeks. All treatment groups were comparable demographically. Primary efficacy measures included total number of panic attacks, global improvement score using the Clinical Global Impressions (CGI) scale, phobic anxiety dimension of the Symptom Checklist-90 phobic cluster, overall phobia state using the Phobia Scale, and severity of illness on the CGI. RESULTS: The 60- and 90-mg/day adinazolam-SR treatment groups showed superior results when compared with the placebo group at Week 4 while the 30-mg group did not. Treatment with adinazolam-SR was well tolerated, with sedation the only treatment-emergent symptom that occurred more frequently in patients treated with adinazolam-SR than placebo. CONCLUSION: These results suggest that adinazolam-SR at doses of 60-mg/day or greater administered twice daily is a safe and effective treatment in selected patients with panic disorder with agoraphobia.

Adolescent↗

PubMed1994

Adinazolam sustained-release treatment of panic disorder: a double-blind study.

Two hundred six outpatients with panic disorder and agoraphobia were randomly assigned to receive 4 weeks of treatment with placebo or sustained-release adinazolam under double-blind conditions. Eighty-eight percent of patients receiving drug and 85% of patients receiving placebo remained in the study at week 4. This report describes the "intent-to-treat" analysis of 202 patients who made at least one follow-up visit after randomization at baseline. On the basis of the Clinical Global Impressions-Improvement Scale, 69.7% of the adinazolam-treated patients were much or very much improved compared with 39.6% of the placebo-treated patients at week 4 or end-point (p = 0.0001). At week 4, panic attacks were completely blocked in 57.1% of adinazolam-treated patients and in 39.2% of the placebo-treated patients (p = 0.009). Adinazolam sustained-release treatment was statistically more effective than placebo treatment on measures of global improvement, number of panic attacks, SCL-90 phobia severity, main phobia severity, and anticipatory and general anxiety. No drug-placebo differences were found for overall self-rated phobia severity, unexpected or situational panic attacks, or for work, family, or social disability.

Adult↗

PubMed1993

Decreased lymphocyte beta-adrenoreceptor function correlates with less agoraphobia and better outcome in panic disorder.

Previous studies have demonstrated reduced function of peripheral beta-adrenoreceptors in panic disorder with agoraphobia (PDA). We recently reported that decreased lymphocyte beta-receptor function was associated with milder agoraphobia and better treatment response in PDA. We now report on lymphocyte beta-receptor function in 12 additional patients with PDA. Lower cyclic AMP responses to isoproterenol were significantly correlated with milder agoraphobia and better response to naturalistic treatment. Lower beta-receptor density tended to correlate similarly with agoraphobia and treatment response. These findings further support the hypothesis that decreased peripheral beta-receptor function in PDA reflects an adaptive process associated with greater resistance to agoraphobia and greater capacity for recovery with treatment.

Adult↗

PubMed1993

Benzodiazepine effects on flicker sensitivity: role of stimulus frequency and size.

1. Benzodiazepines (BZDs) impair sensitivity to temporally modulated visual stimuli (flicker). Critical flicker-fusion frequency (CFF) is commonly used as a measure of this effect, but it only measures sensitivity to a narrow range of frequencies, usually above 25 Hz. Are other frequencies more sensitive to the effects of BZDs? 2. Flicker sensitivity at 1, 2, 4, 8, 16, and 32 Hz was measured for 1 degrees and 5 degrees stimuli before and 50 to 100 minutes after triazolam (0.25 mg), lorazepam (1.0 mg) and placebo. Drug effects on CFF were also measured. 3. Both BZDs significantly impaired overall flicker sensitivity. Triazolam produced 50% more impairment than lorazepam. CFF was significantly impaired by triazolam. BZD effects did not vary with stimulus size. 4. Significantly greater BZD-induced impairment of flicker sensitivity occurred at 16 Hz than at 1, 2, 4, or 32 Hz. 5. The magnitude of BZD effects on flicker sensitivity vary with the temporal frequency of the stimulus. BZD effects are greatest for 8-16 Hz stimuli.

Adult↗

PubMed1993

Evidence that decreased function of lymphocyte beta adrenoreceptors reflects regulatory and adaptive processes in panic disorder with agoraphobia.

OBJECTIVE: This study was designed to clarify the nature of the reduced function of the peripheral beta adrenoceptor system observed in panic disorder with agoraphobia. The authors hypothesized that this phenomenon reflected a regulatory and adaptive process. METHODS: Lymphocyte beta adrenoreceptor density and affinity, basal lymphocyte cAMP level, and isoproterenol-stimulated cAMP generation were measured in 27 untreated outpatients with panic disorder with agoraphobia and 24 healthy comparison subjects. Lymphocyte beta receptor attributes were again assessed in patients after 4 weeks of double-blind treatment with adinazolam (slow-release form) or placebo. Panic frequency, agoraphobic symptoms, overall anxiety, and improvement with treatment were assessed with standard rating instruments. RESULTS: Multivariate statistics revealed significantly lower beta receptor density and isoproterenol-stimulated cAMP generation in patients than in comparison subjects. beta receptor density tended to normalize after adinazolam but not after placebo. Pretreatment beta receptor density was lower in treatment responders than nonresponders. Patients with mild agoraphobia had lower cAMP responsivity than patients with moderate or severe agoraphobia. CONCLUSIONS: Decreased function of lymphocyte beta receptors in panic disorder with agoraphobia is expressed as both decreased density and decreased cAMP responsivity. This pattern of changes, and the tendency for receptor density to normalize with treatment, is consistent with an active, regulatory process rather than a structural deficit in the beta receptor system. Preliminary clinical findings suggest that these changes may reflect adaptive processes associated with a favorable clinical course in panic disorder with agoraphobia.

Adult↗

PubMed1993

Relationships between thyroid indices and symptoms of anxiety in depressed outpatients.

Scores on rating scales measuring symptoms of depression, panic anxiety, state anxiety, trait anxiety, and agoraphobic avoidance were correlated, using multivariate statistics, with total thyroxine- and thyrotropin-releasing hormone concentrations in outpatients with major depression. A significant inverse relationship was demonstrated between agoraphobic avoidance and total thyroxine concentrations in female patients. No other symptom ratings were significantly associated with these thyroid indices. The depressed patients scored in the clinically significant range for agoraphobic symptoms. Assessment of agoraphobic avoidance may help identify a clinically and biologically distinct subgroup of depressed patients.

Adult↗

PubMed1993

Relationship of past depressive episodes to symptom severity and treatment response in panic disorder with agoraphobia.

BACKGROUND: Many investigators have reported that panic disorder (PD) patients with comorbid major depression (MD) have more severe symptoms and a poorer response to treatment than patients with PD alone. It is not known if this is due to a distinct and more serious underlying disorder in these patients or simply a result of the simultaneous presence of the two disorders. METHOD: Nondepressed patients presenting for treatment of panic disorder with agoraphobia (PDA) were studied before treatment (N = 180) and after 4 weeks of treatment with adinazolam sustained release (N = 89) or placebo (N = 91). Twenty-nine percent (N = 53) of the patients had a past history of MD. Symptom severity and treatment outcome were compared in patients with primary, secondary, single, recurrent, or no past MD. RESULTS: There were no consistent differences in symptom severity or treatment outcome in patients with a past history of primary, secondary, or single episode MD compared with patients with no history of MD. However, a small number of patients with history of recurrent MD exhibited consistently greater symptom severity and poorer response to treatment than patients with no history of MD. CONCLUSION: The greater severity and worse outcome of comorbid PD and MD observed in earlier studies are more likely due to the simultaneous presence of the two disorders than to a more serious and enduring underlying disorder. However, our results suggest that recurrent MD may indicate a more serious condition in patients with PDA. This possibility warrants further study.

Adult↗

PubMed1992

Imipramine and alprazolam effects on stress test reactivity in panic disorder.

The reactivity of 40 panic disorder patients on mental arithmetic, cold pressor, and 5% CO2 inhalation stressors was tested before and after 8 weeks of treatment with imipramine, alprazolam, or placebo. Mean levels of subjective and physiological stress measures were compared during a baseline before any stressors were given, and at anticipation, stressor, and recovery periods for each stressor. After treatment, imipramine patients differed from the other two treatment groups on the prestressor baseline in showing higher systolic blood pressure (mean difference about 10 mmHg), higher diastolic blood pressure (10 mm Hg), higher heart rate (15 bpm), less respiratory sinus arrhythmia, shorter pulse transit time, and lower T-wave amplitude. Respiratory measures, electrodermal measures, body movement, and self-reported anxiety and excitement did not distinguish the groups. Reactivity to the stress tests was unaffected by the medications, but tonic differences present in the baseline persisted.

Adult↗

PubMed1992

Stress test reactivity in panic disorder.

The psychological and physiological reactivity of 52 patients with panic disorder to mental arithmetic, cold pressor, and 5% carbon dioxide inhalation tests was compared with that of 26 age- and sex-matched normal subjects. In general, patients with panic disorder were neither more physiologically reactive to these stressors than normal subjects nor slower to recover from them, but they were tonically more anxious and much more likely to ask to stop carbon dioxide inhalation or to report panic attacks during this test. Patients who reported panic attacks (46%) had manifested greater anticipatory anxiety before the gas was delivered, accompanied with increased beta-adrenergic cardiac tone. Thus, anticipatory anxiety can be an important factor in panic provocation. Physiological measures varied greatly in their sensitivity to phasic or tonic anxiety. Carbon dioxide stimulated large increases in respiratory minute volume, but these increases were no greater for patients than for normal subjects.

Adult↗

PubMed1992

Patterns of abnormal processing of emotional information in panic disorder and major depression.

Studies showing interference with color naming threat-related words in patients with anxiety disorders suggest a bias towards processing threatening material in these patients. We assessed the specificity of this finding to anxiety disorders and to threatening stimuli by administering Stroop cards with a variety of types of emotional stimuli to 24 panic disorder patients with no history of major depression, 30 patients with major depression and no history of panic attacks and 25 controls with no history of an axis I disorder. Our findings suggest that the abnormal information processing seen in panic disorder may be characterized by a more general bias towards processing emotional stimuli than previously thought. They also suggest that this more general bias may illustrate differences in information processing in panic disorder and major depression.

Adult↗

PubMed1992

Chest pain in generalized anxiety disorder.

OBJECTIVES: The objectives of the current study were to evaluate the prevalence of chest pain and related medical utilization in patients with generalized anxiety disorder and to investigate the possible relationship between the occurrence of chest pain in these patients and the episodes of excessive worry which characterize this disorder. METHOD: The presence of a history of chest pain in patients with generalized anxiety disorder was investigated in an outpatient psychiatric sample using a structured interview which also assessed related medical utilization and the relationship of chest pain to panic attacks and episodes of excessive worry. RESULTS: Of fifty sequentially evaluated patients meeting DSM-III R criteria for G.A.D., twenty-four (48%) reported a history of chest pain. Seven of these patients also had a history of panic attacks, however, four of the seven reported that their pain occurred independently of their panic attacks. Sixteen patients with G.A.D. reported that their chest pain episodes were associated with episodes of excess worry. Eleven had sought medical evaluation for their pain. Patients with chest pain and normal coronary arteries are frequently found to have panic disorder. The pattern of utilization of medical care was comparable in this sample of patients with G.A.D. and a group of patients with panic disorder recruited in a similar manner. CONCLUSIONS: These results suggest that in addition to panic disorder, G.A.D. may also be a common diagnosis in chest pain patients with no demonstrable coronary disease. Future studies of coronary artery disease negative patients with chest pain should include assessments for the presence of G.A.D. Our results also suggest that chest pain may be a common symptom in G.A.D. The possibility that chest pain should be included in the diagnostic criteria for this disorder should be the subject of further investigation.

Adult↗

PubMed1991

Hyperventilation-induced panic attacks in panic disorder with agoraphobia.

Eight minutes of hyperventilation to an end-tidal PCO2 of less than 20 mmHg led to a panic attack in 7 of 12 patients with panic disorder with agoraphobia and only 1 of 12 normal controls. Patients experienced greater increases in panic symptoms than controls during hyperventilation. Patients who reported more distress from somatic symptoms of hyperventilation during the preceding week were more likely to panic during hyperventilation. Patients who panicked during hyperventilation exhibited a delayed recovery of normocapnia following hyperventilation. Hyperventilation by this protocol is an effective means of inducing panic attacks in the laboratory. A hyperventilation challenge may identify a subgroup of patients for whom hyperventilation symptoms are frequently associated with panic.

Adult↗

PubMed1991

Elevated serum lactate associated with panic attacks induced by hyperventilation.

Several lines of evidence suggest that lactate metabolism may be altered in panic disorder. We recently reported exaggerated increases in serum lactate in panic patients following hyperventilation during glucose infusion. In the current study, lactate metabolism was stimulated by hyperventilation following glucose ingestion in 12 panic patients and 12 controls. The seven patients who panicked during hyperventilation exhibited larger increases in serum lactate levels than nonpanicking patients or controls. The lactate response was significantly correlated with peak ratings of anxiety and panic symptoms, but not correlated with insulin or cortisol levels, heart rate, pCO2, adiposity, exercise habits, or diet. Hyperventilation-induced panic appears to be associated with metabolic changes leading to elevated serum lactate.

Adult↗

PubMed1991

Beta receptor density in human lymphocyte membranes: changing with aging?

The number of beta adrenergic binding sites (Bmax) in human lymphocyte membranes has been reported to decrease, remain the same, or increase with age. In order to address this issue, we used two highly specific beta receptor ligands with lymphocytes from healthy aged (range: 51-90 years) and young (19-39 years) subjects in two separate studies. Because depression can reduce Bmax, potential aged subjects were excluded if they had high scores on tests for depression. Bmax was higher in the aged group of each study (33% higher in the first, p less than .01, and 72.5% in the second, p less than .02); the results were similar in both studies. Antagonist affinity did not differ between young and aged groups in either study. We suggest that some of the discrepancies in the literature could be due to differences in age ranges used or to inclusion of depressed subjects in prior studies.

Adrenergic beta-Antagonists↗

PubMed1991

Response to treatment in panic disorder with associated depression.

Thirty outpatients with panic disorder (PD) were treated at an anxiety clinic using a symptom-focused approach. Thirteen (43%) had no history of major depressive disorder (MDD), 12 (40%) had a history of secondary MDD, and 5 (17%) had history of primary MDD. The outcome was equally good in patients with no history of MDD (77% had good or excellent outcomes) and patients with a history of secondary MDD (83% had good or excellent outcomes). Patients with a history of primary MDD had the worst outcomes. These findings agree with earlier studies showing that secondary MDD does not adversely affect prognosis of patients presenting for treatment of PD.

Adult↗

PubMed1990

Elevated serum lactate following hyperventilation during glucose infusion in panic disorder.

Early investigators reported that patients with anxiety syndromes associated with panic attacks produced more lactate during exercise than control subjects. These studies suggested a metabolic difference between patients and controls. However, the possibility that patients were simply less fit than controls could not be excluded. In this study, serum lactate was measured in panic disorder patients in response to a metabolic challenge not involving exercise. Voluntary hyperventilation during iatrogenic hyperglycemia led to an increase in serum lactate. The increase in serum lactate was significantly greater in panic disorder patients than in controls. Hyperventilation provoked panic attacks in 4 of 8 patients and none in 6 controls. There was no evidence of a relationship between the increase in lactate or the associated decrease in phosphate and the level of anxiety produced by this procedure.

Adult↗

PubMed1989

Lymphocyte beta-adrenoreceptor density in patients with unipolar depression and normal controls.

Values of binding maximum (Bmax) and dissociation constant (Kd) of (-)3-[125I]iodocyanopindolol (ICYP) were determined in beta-adrenergic receptors of membranes of peripheral lymphocytes in 32 patients with unipolar depression (DSM-III-R) and 31 normal controls. Results were analyzed by a two-way Analysis of Covariance method. A significant difference was noted for group assignment (patient versus control, p less than 0.05). Mean Bmax (fmol ICYP bound/mg lymphocyte membrane fraction total protein) of patients was 31.9 +/- 3.84 (SE) and controls 46.3 +/- 3.92 (SE). A significant interaction was found between group membership and gender (p less than 0.05). In the female patient group (n = 14), mean Bmax was 30.5 +/- 5.79 (SE); in female controls, mean Bmax was 56.0 +/- 5.15 (SE). Differences between male patients and male controls were not significant. Mean values of Kd (pmol/liter) showed a trend for patient values to be lower than control values [69.0 +/- 13.66 (SE) versus 108.5 +/- 14.42 (SE), respectively]. A significant inverse relationship was noted between lymphocyte beta-receptor Bmax and frequency of panic attacks during the depressive episode in 18 patients (p = 0.05). No relationship was found between values of Kd and frequency of panic attacks in these patients. Thus, preliminary evidence is provided for relationships among altered beta-adrenergic receptor binding, gender, and indices of panic-anxiety in unipolar depressed patients.

Adult↗