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Dive into the research topics where Stuart A. Checkley is active.

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Featured researches published by Stuart A. Checkley.


Biological Psychiatry | 2003

Neural abnormalities during cognitive generation of affect in Treatment-Resistant depression

Veena Kumari; Martina Mitterschiffthaler; John D. Teasdale; Gin S. Malhi; Richard G. Brown; Vincent Giampietro; Michael Brammer; Lucia Poon; Andrew Simmons; Steven Williams; Stuart A. Checkley; Tonmoy Sharma

BACKGROUND Dysfunctions in brain regions known to be involved in affect and mood states are thought to be implicated in depression and may have a role in determining the type and symptoms of this illness. METHODS Functional magnetic resonance imaging was used to elucidate neural correlates of cognitive generation of affect, using a previously published paradigm of evoking affect with picture-caption pairs, in patients with unipolar, treatment-resistant depression. RESULTS Compared with control participants, patients showed relatively decreased response in the anterior cingulate (rostral; right) with both negative and positive picture-caption pairs and in the medial frontal gyrus and hippocampus (all left) with positive picture-caption pairs. They demonstrated increased response in the inferior (right) and middle temporal gyri (left) with negative picture-caption pairs, and in the parahippocampal gyrus (right), inferior frontal gyrus (left), subgenual cingulate (right), striatum (right), and brain stem (left) with positive picture-caption pairs. CONCLUSIONS Reduced medial/middle prefrontal and hippocampal activity may account for positive affect disturbances and temporal lobe hyperactivity for negative affect disturbances in treatment-resistant depression. The results also corroborate previous observations from resting positron emission tomography studies and further elucidate the association between hypoactive rostral cingulate and nonresponsiveness to treatment in depression.


Psychopharmacology | 1996

Effect of cigarette smoking on prepulse inhibition of the acoustic startle reflex in healthy male smokers.

Veena Kumari; Stuart A. Checkley; Jeffrey A. Gray

Abstract The present study investigated the effects of cigarette smoking on prepulse inhibition (PPI) of the acoustic startle reflex in healthy men. Cigarette smoking in a group of overnight smoking-deprived smokers increased PPI as compared to the smoking-deprived condition. This finding is consistent with previous animal studies showing that nicotine increases PPI of the acoustic startle reflex. In addition, cigarette smoking also reduced startle amplitude during the first 6–7 min of the post-smoking session.


Journal of Affective Disorders | 1995

Treatment of Major Depression with metyrapone and hydrocortisone

A.-M. O'Dwyer; S.L. Lightman; M.N. Marks; Stuart A. Checkley

Eight inpatients with Major Depression were treated with metyrapone and hydrocortisone in a balanced order placebo-controlled single-blind cross-over study. The hydrocortisone dose (30 mg daily) was a physiological replacement dose and the metyrapone dose was titrated against plasma cortisol in order to keep cortisol within physiological limits. The treatment resulted in a significant reduction in depressive symptoms. This placebo-controlled study replicates the results of several uncontrolled studies but leaves open for further study the mechanism by which the combined administration of metyrapone and hydrocortisone might exert its antidepressant effect.


Psychopharmacology | 1997

Effect of acute subcutaneous nicotine on prepulse inhibition of the acoustic startle reflex in healthy male non-smokers

Veena Kumari; Paul A. Cotter; Stuart A. Checkley; Jeffrey A. Gray

Abstract In a double-blind placebo-controlled trial, the effects of two doses (6 μg/kg, 12 μg/kg) of acute SC nicotine were investigated on prepulse inhibition (PPI) of the acoustic startle reflex in healthy non-smoker male volunteers. Each subject received three injections [placebo (saline), 6 μg/kg nicotine, 12 μg/kg nicotine] on separate occasions, 2 weeks apart. No influence of either 6 μg/kg or 12 μg/kg nicotine was observed for the amplitude and habituation of the startle response over pulse-alone stimuli, relative to the saline-treated condition. Percent of PPI (expressed as percent reduction of non-prepulse trials) was significantly greater, but PPI as measured by absolute difference scores was not significantly different, when subjects were given the 12 μg/kg dose of nicotine than saline. There was an increase in percent of PPI from saline through low to high doses of nicotine, but PPI observed under the low dose did not differ significantly from either the high dose or placebo. These results provide some support for previous findings showing an enhancement in PPI by cigarette smoking in overnight smoking-deprived smokers and by acutely administered nicotine in experimental animals. The findings indicate that previously observed effects of smoking on percent of PPI in smoking-deprived subjects were not attributable to the restoration of a deficit induced by smoking withdrawal, but represent a direct pharmacological action of nicotine.


Personality and Individual Differences | 1995

PERSONALITY AND AFFECTIVE MODULATION OF THE STARTLE REFLEX

Philip J. Corr; Glenn D. Wilson; Maria Fotiadou; Veena Kumari; Nicola S. Gray; Stuart A. Checkley; Jeffrey A. Gray

Abstract The human startle reflex, as indexed by strength of eyeblink to a sudden, loud noise, has been shown to vary according to the presence of pleasant and unpleasant stimuli. An experiment was conducted to determine whether this effect is in turn dependent on the personality of the subject. Subjects viewed a series of slides classified as pleasant, unpleasant or neutral, with acoustic startle probes being presented unpreditably during and between slides. Electromyographic (EMG) measures of eyeblink responses confirmed the expected pattern of modulation, with pleasant slides reducing and unpleasant slides increasing the amplitude of startle. Harm Avoidance (HA), as measured by Cloningers Tridimensional Personality Questionnaire (TPQ), mediated these effects: only subjects high in HA showed modulation to unpleasant slides, while only subjects low in HA showed modulation to pleasant slides. Affective modulation, as measured by response latency, was mediated by Extraversion (E) and Neuroticism (N), as measured by the Eysenck Personality Questionnaire (EPQ): only subjects who were extraverted and stable showed the expected linear pattern of modulated startle. The implications of these data for Cloningers. Grays and Eysencks theories of personality are discussed.


Journal of Psychopharmacology | 1999

effects of d-amphetamine and haloperidol on latent inhibition in healthy male volunteers

Veena Kumari; Paul A. Cotter; Owen F. Mulligan; Stuart A. Checkley; Nicola S. Gray; David R. Hemsley; Jasper C. Thornton; Philip J. Corr; Brian Toone; Jeffrey A. Gray

Latent inhibition (LI) refers to a retardation of learning about the consequences of a stimulus when that stimulus has been passively presented a number of times without reinforcement. Acute positive-symptom schizophrenics, normal volunteers who score high on questionnaire measures of schizotypy and non-patients or animals treated with dopamine agonists show reduced LI. Neuroleptic drugs, such as haloperidol, administered at low doses, potentiate LI and effectively reverse disruption of LI induced by dopamine agonists in animals. However, a high dose of haloperidol, administered on its own, has been found to reduce LI. We examined the effects on LI of acute oral administration of an indirect dopamine-agonist, d-amphetamine (5 mg), and a nonselective dopamine receptor antagonist, haloperidol (5 mg), in normal male volunteers, using an associative learning task. Replicating previous reports, we found that d-amphetamine reduced LI; haloperidol also reduced LI, but only in subjects who scored low on the Psychoticism scale of the Eysenck Personality Questionnaire. In a subsequent study, no effect was found of 2 mg oral haloperidol administration on LI. The effect of 5 mg haloperidol on LI is interpreted as similar to that observed with a high dose of haloperidol in rats.


Journal of Affective Disorders | 2003

Response style, interpersonal difficulties and social functioning in major depressive disorder

Dominic Lam; Nikki Schuck; Neil Smith; Anne Farmer; Stuart A. Checkley

BACKGROUND It is postulated that depressed patients who engaged in self-focused rumination on their depressive symptoms may experience more hopelessness, more interpersonal distress and poorer social functioning while patients who distract themselves may experience less severe hopelessness and better social functioning. METHOD One-hundred and nine outpatients suffering from DSM-IV (APA, 1994) major depressive disorders filled in questionnaires that mapped into their response style to depression, hopelessness and interpersonal style. They were also interviewed for their levels of social functioning. RESULTS Rumination was associated with higher levels of depression and distraction was associated with lower levels of depression. Furthermore when levels of depression and gender were controlled for, rumination contributed to higher levels of hopelessness and distraction contributed to lower levels of hopelessness. Both rumination and levels of depression contributed significantly to higher levels of interpersonal distress when gender was controlled for. Ruminators were rated to have significantly more severe problems in intimate relationships while distractors were rated to have significantly higher social functioning. CONCLUSION Our study suggests the importance of teaching patients techniques to distract themselves. This could prevent patients from getting into a vicious cycle of self-absorption and increased levels of hopelessness, finding it hard to interact with people in their social network and neglecting their intimate relationships.


Psychoneuroendocrinology | 1996

The relationship between the effects of metyrapone treatment on depressed mood and urinary steroid profiles

P.W. Raven; A.-M. O'Dwyer; Norman F. Taylor; Stuart A. Checkley

In order to investigate mechanisms by which the adrenal 11 beta-hydroxylase inhibitor metyrapone might exert its antidepressant effect, we used gas chromatography to analyse the 24 h urinary steroid profiles from six females with major depression taking part in a trial of metyrapone (2-4 g/day) as an antidepressant. Due to concurrent administration of hydrocortisone (30 mg/day), plasma cortisol levels were not significantly reduced. Treatment with metyrapone resulted in greatly increased urinary excretion of 11-deoxy corticosteroids, including the GABA-modulatory steroid tetrahydro-11-deoxycorticosterone (from 68 +/- 34 to 219 +/- 75 micrograms/24 h, p < .05). Metyrapone also had multiple extra-adrenal effects on corticosteroid metabolism, including inhibition of the peripheral conversion of cortisone to cortisol as demonstrated by a significant decrease in the ratio of 11 beta-hydroxy/11-oxo metabolites of cortisol (from 0.81 +/- 0.08 to 0.46 +/- 0.04, p < .01). The decreased Montgomery-Asberg Depression Rating Scale scores seen during treatment with metyrapone did not correlate with changes in plasma cortisol, but did correlate significantly with total 11-deoxycortisol metabolites (r = 0.778, n = 12, p < .01). We conclude that, in addition to decreased cortisol synthesis, increased secretion of cortisol precursors and reduced local bioavailability of cortisol may play a role in the antidepressant effect of metyrapone.


Psychopharmacology | 1997

Effects of acute administration of d-amphetamine and haloperidol on procedural learning in man.

Veena Kumari; Jeffrey A. Gray; Philip J. Corr; Owen F. Mulligan; Paul A. Cotter; Stuart A. Checkley

The effects of an indirect dopamine-agonist, d-amphetamine, and a non-selective dopamine receptor antagonist, haioperidol, were investigated in normal male volunteers using a between-subjects double-blind design in a procedural learning task, thought mainly to involve unconscious/automatic learning. The results showed: (1) d-amphetamine facilitated response speed, whereas haioperidol inhibited it, in comparison to placebo; (2) the linear increase in procedural learning corresponded with pharmacological manipulation of degree of dopaminergic activity, i.e. subjects given haioperidol showed the least, and subjects given d-amphetamine the greatest, procedural learning. The implications of these findings are discussed in relation to investigation of abnormalities of procedural learning processes in schizophrenia.


Behavioural Pharmacology | 1998

Effects of single oral administrations of haloperidol and d-amphetamine on prepulse inhibition of the acoustic startle reflex in healthy male volunteers

Veena Kumari; Owen F. Mulligan; Paul A. Cotter; L. Poon; Brian Toone; Stuart A. Checkley; Jeffrey A. Gray

The effects of acute administration of an indirect dopamine-agonist, d-amphetamine, and a non-selective dopamine receptor antagonist, haloperidol, were investigated in normal male volunteers on habituation and prepulse inhibition (PPI) of the acoustic startle reflex in two experiments. In Experiment 1, 40 male non–smoker volunteers were tested for habituation and PPI (defined as percentage reduction of the pulse-alone amplitude; prepulses 9 dB above background) before and after double–blind administration of either 2mg haloperidol or placebo. No influence of haloperidol was observed on either habituation or PPI of the startle reflex in this experiment. In Experiment 2, 60 male volunteers underwent startle testing before and after double-blind administration of a single oral dose of 5 mg haloperidol, 5 mg damphetamine or placebo. Habituation and PPI (prepulses 15 dB above background) for the placebo group did not differ significantly from that observed for the rf-amphetamine or for the haloperidol group. However, in a subgroup of smoking subjects, both d-amphetamine and haloperidol reduced PPI as compared to that observed prior to drug administration. The implications of these findings in relation to animal pharmacological studies and observed sensorimotor gating deficits in schizophrenia are discussed. Behav Pharmacol 1998; 9:567— 576

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C Franey

King's College London

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L. Poon

South London and Maudsley NHS Foundation Trust

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