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Dive into the research topics where Gary E. Cordingley is active.

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Featured researches published by Gary E. Cordingley.


Headache | 2000

Psychosocial correlates and impact of chronic tension-type headaches.

Kenneth A. Holroyd; Michael D. Stensland; Kimberly R. Hill; Francis S. O'Donnell; Gary E. Cordingley

Objectives.– To examine the psychosocial correlates of chronic tension‐type headache and the impact of chronic tension‐type headache on work, social functioning, and well‐being.


Headache | 1991

Propranolol in the management of recurrent migraine : a meta-analytic review

Kenneth A. Holroyd; Donald B. Penzien; Gary E. Cordingley

SYNOPSIS


BMJ | 2010

Effect of preventive (β blocker) treatment, behavioural migraine management, or their combination on outcomes of optimised acute treatment in frequent migraine: randomised controlled trial

Kenneth A. Holroyd; Constance K. Cottrell; O'Donnell Fj; Gary E. Cordingley; J. Drew; Bruce W. Carlson; Lina K. Himawan

Objective To determine if the addition of preventive drug treatment (β blocker), brief behavioural migraine management, or their combination improves the outcome of optimised acute treatment in the management of frequent migraine. Design Randomised placebo controlled trial over 16 months from July 2001 to November 2005. Setting Two outpatient sites in Ohio, USA. Participants 232 adults (mean age 38 years; 79% female) with diagnosis of migraine with or without aura according to International Headache Society classification of headache disorders criteria, who recorded at least three migraines with disability per 30 days (mean 5.5 migraines/30 days), during an optimised run-in of acute treatment. Interventions Addition of one of four preventive treatments to optimised acute treatment: β blocker (n=53), matched placebo (n=55), behavioural migraine management plus placebo (n=55), or behavioural migraine management plus β blocker (n=69). Main outcome measure The primary outcome was change in migraines/30 days; secondary outcomes included change in migraine days/30 days and change in migraine specific quality of life scores. Results Mixed model analysis showed statistically significant (P≤0.05) differences in outcomes among the four added treatments for both the primary outcome (migraines/30 days) and the two secondary outcomes (change in migraine days/30 days and change in migraine specific quality of life scores). The addition of combined β blocker and behavioural migraine management (−3.3 migraines/30 days, 95% confidence interval −3.2 to −3.5), but not the addition of β blocker alone (−2.1 migraines/30 days, −1.9 to −2.2) or behavioural migraine management alone (−2.2 migraines migraines/30 days, −2.0 to −2.4), improved outcomes compared with optimised acute treatment alone (−2.1 migraines/30 days, −1.9 to −2.2). For a clinically significant (≥50% reduction) in migraines/30 days, the number needed to treat for optimised acute treatment plus combined β blocker and behavioural migraine management was 3.1 compared with optimised acute treatment alone, 2.6 compared with optimised acute treatment plus β blocker, and 3.1 compared with optimised acute treatment plus behavioural migraine management. Results were consistent for the two secondary outcomes, and at both month 10 (the primary endpoint) and month 16. Conclusion The addition of combined β blocker plus behavioural migraine management, but not the addition of β blocker alone or behavioural migraine management alone, improved outcomes of optimised acute treatment. Combined β blocker treatment and behavioural migraine management may improve outcomes in the treatment of frequent migraine. Trial registration Clinical trials NCT00910689.


Journal of Consulting and Clinical Psychology | 1991

A comparison of pharmacological (amitriptyline HCL) and nonpharmacological (cognitive-behavioral) therapies for chronic tension headaches

Kenneth A. Holroyd; Justin M. Nash; Jeffrey D. Pingel; Gary E. Cordingley; Albert Jerome

Forty-one recurrent tension headache sufferers were randomly assigned to either cognitive-behavioral therapy (administered in a primarily home-based treatment protocol) or to amitriptyline therapy (with dosage individualized at 25, 50, or 75 mg/day). Cognitive-behavioral therapy and amitriptyline each yielded clinically significant improvements in headache activity, both when improvement was assessed with patient daily recordings (56% and 27% reduction in headache index, respectively), and when improvement was assessed with neurologist ratings of clinical improvement (94% and 69% of patients rated at least moderately improved, respectively). In instances where differences in treatment effectiveness were observed (headache index, somatic complaints, perceptions of control of headache activity), cognitive-behavioral therapy yielded somewhat more positive outcomes than did amitriptyline. Neither treatment, however, eliminated headache problems.


Pain | 1996

Central and peripheral mechanisms in chronic tension-type headache.

Kenneth A. Holroyd; Steven Kvaal; David Segal; Gary E. Cordingley; Lori A. Rokicki; McCool Hr

&NA; The second exteroceptive suppression of masseter muscle activity (ES2) and tenderness in pericranial muscles were evaluated in 112 young adults who met IRS criteria in the following diagnostic classifications: 31 chronic tension headache, 31 episodic tension headache, 33 migraine without aura and 17 migraine with aura. An additional 31 subjects served as controls. Pericranial muscle tenderness better distinguished diagnostic subgroups and better distinguished recurrent headache sufferers from controls than did masseter ES2. Chronic tension headache sufferers exhibited the highest pericranial muscle tenderness, and controls exhibited the lowest tenderness (P < 0.01). All chronic tension headache sufferers exhibited muscle tenderness in at least one of the pericranial muscles evaluated, while tenderness was exhibited by 52% of controls. The association between pericranial muscle tenderness and chronic tension headache was independent of the intensity, frequency, or chronicity of headaches. Our findings raise the possibility that pericranial muscle tenderness is present early in the development of tension headache, while ES2 suppression only emerges later in the evolution of the disorder.


Journal of Consulting and Clinical Psychology | 1995

Enhancing the Effectiveness of Relaxation--Thermal Biofeedback Training with Propranolol Hydrochloride.

Kenneth A. Holroyd; Gary E. Cordingley; Lori A. Rokicki; Steven Kvaal; Lipchik Gl; McCool Hr

This article evaluated the ability of propranolol to enhance results achieved with relaxation-biofeedback training. Thirty-three patients were randomized to relaxation-biofeedback training alone (administered in a limited-contact treatment format), or to relaxation-biofeedback training accompanied by long-acting propranolol (with dosage individualized at 60, 120, or 180 mg/day). Concomitant propranolol therapy significantly enhanced the effectiveness of relaxation-biofeedback training when either daily headache recordings (79% vs. 54% reduction in migraine activity) or neurologist clinical evaluations (90% vs. 66% reduction) were used to assess treatment outcome. Concomitant propranolol therapy also yielded larger reductions in analgesic medication use and greater improvements of quality of life measures than relaxation-biofeedback training alone but was more frequently associated with side effects.


Headache | 1989

Enhancing the Effectiveness of Abortive Therapy: A Controlled Evaluation of Self-Management Training

Kenneth A. Holroyd; Gary E. Cordingley; Jeffrey D. Pingel; Albert Jerome; Angelo G. Theofanous; David K. Jackson; B A Leland Leard

SYNOPSIS


Headache | 2003

Treating Chronic Tension‐type Headache Not Responding to Amitriptyline Hydrochloride With Paroxetine Hydrochloride: A Pilot Evaluation

Kenneth A. Holroyd; Jennifer S. Labus; Francis J. O'Donnell; Gary E. Cordingley

Context.—In some individuals, chronic tension‐type headache fails to respond to tricyclic antidepressant medications that often serve as first‐line therapy.


Applied Psychophysiology and Biofeedback | 1989

Long-term maintenance of improvements achieved with (abortive) pharmacological and nonpharmacological treatments for migraine: preliminary findings.

Kenneth A. Holroyd; Jeffrey F. Holm; Donald B. Penzien; Gary E. Cordingley; Karl G. Hursey; Nancy J. Martin; Angelo G. Theofanous

This report presents the first prospective comparison of the long-term maintenance of reductions in recurrent migraine headaches achieved with (abortive) pharmacological and nonpharmacological (combined relaxation training and thermal biofeedback training) treatments. Nineteen of 21 (90%) successfully treated patients (50% or greater reduction in headache activity) were contacted for follow-up evaluation 3 years later. Migraine sufferers who had been treated with ergotamine were less likely to still be relying on the treatment they had received and more likely to have additional medical treatment for their headaches and to be using prophylactic or narcotic medication than were migraine sufferers who had been treated with relaxation/biofeedback training. However, daily headache recordings revealed that patients in both treatment groups continued to show lower headache activity at 3-year follow-up than prior to treatment. Although preliminary, these findings raise the possibility that improvements achieved with nonpharmacological treatment are more likely to be maintained without additional treatment than are similar improvements achieved with abortive pharmacological treatment.


American Journal of Emergency Medicine | 1993

Increases in serum prolactin levels associated with syncopal attacks.

Gary E. Cordingley; David M. Brown; Peter Dane; Karl Harnish; Paul Cadamagnani; Thomas H. O'Hare

Numerous investigators have found that serum prolactin levels increase after tonic-clonic and partial complex seizures, but the effect of syncope on prolactin levels has been studied little. Serum prolactin levels were measured following unexpected syncopal attacks in patients seeking emergency treatment in a community hospital. Levels sampled 18 to 60 minutes after syncopal episodes were increased in 8 of 11 cases. Follow-up prolactin levels, measured 17 to 222 days later, were normal in all eight cases in which they were initially increased. Most subjects had concurrent illness. Although the current study does not clarify whether it was the syncope, the concurrent illness, or both that caused the prolactin elevations, it implies that measurement of this hormone will not help the clinician in distinguishing between seizures and syncopal attacks.

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Donald B. Penzien

University of Mississippi Medical Center

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