Depression: McAllister-Williams RH

Anderson IM, Ferrier IN, Baldwin RC, Cowen PJ, Howard L, Lewis G, Matthews K, McAllister-Williams RH, Peveler RC, Scott J, Tylee A. · Senior Lecturer and Honorary Consultant Psychiatrist, Neuroscience and Psychiatry Unit, University of Manchester, UK. · J Psychopharmacol. · Pubmed #18413657 No free full text.

Abstract: A revision of the 2000 British Association for Psychopharmacology evidence-based guidelines for treating depressive disorders with antidepressants was undertaken to incorporate new evidence and to update the recommendations where appropriate. A consensus meeting involving experts in depressive disorders and their management was held in May 2006. Key areas in treating depression were reviewed, and the strength of evidence and clinical implications were considered. The guidelines were drawn up after extensive feedback from participants and interested parties. A literature review is provided, which identifies the quality of evidence to inform the recommendations, the strength of which are based on the level of evidence. These guidelines cover the nature and detection of depressive disorders, acute treatment with antidepressant drugs, choice of drug versus alternative treatment, practical issues in prescribing and management, next-step treatment, relapse prevention, treatment of relapse, and stopping treatment.

McAllister-Williams RH. · No affiliation provided · Br J Hosp Med (Lond). · Pubmed #18557543 No free full text.

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McAllister-Williams RH. · No affiliation provided · Br J Hosp Med (Lond). · Pubmed #16498902 No free full text.

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Palaniyappan L, McAllister-Williams RH. · Institute of Neuroscience, Newcastle University, Royal Victoria Infirmary, Newcastle upon Tyne. · Br J Hosp Med (Lond). · Pubmed #18386732 No free full text.

Abstract: Depression is one of the most common mental illnesses and has a high impact on individuals and society. Despite the numerous treatment approaches, poor response combined with the burden of residual symptoms negatively affects the overall outcome. Novel pharmacological approaches could help to address this issue.

Corcoran C, McAllister-Williams RH. · Clinical Psychopharmacology and Honorary Consultant Psychiatrist, School of Neurology, Neurobiology and Psychiatry, Royal Victoria Infirmary, Newcastle upon Tyne. · Br J Hosp Med (Lond). · Pubmed #17663313 No free full text.

Abstract: Depression is a serious illness associated with morbidity and mortality, but it is treatable. However, outcomes are often far from ideal with patients left with residual symptoms of depression. These are associated with poor social functioning and an increased risk of relapse.

McAllister-Williams RH. · School of Neuroscience and Psychiatry, University of Newcastle, Newcastle upon Tyne, UK. · J Psychopharmacol. · Pubmed #16551667 No free full text.

Abstract: Bipolar disorder is an important and serious mental illness associated with significant morbidity and mortality. However, unfortunately, the evidence base regarding treatment is less than satisfactory. In such circumstances clinicians often resort to reputable sets of guidelines. A number of these currently exist; in the United Kingdom the most prominent being that produced by the British Association of Psychopharmacology (BAP). This paper reviews the methodology of this guideline and its recommendations regarding the long-term treatment of bipolar disorder and compares this with guidelines produced by the American Psychiatric Association (APA), the Canadian Network for Mood and Anxiety Treatments (CANMAT) and the Texas Implementation of Medication Algorithms (TIMA) for bipolar I disorder. It is concluded that the BAP guidelines continue to be a reasonable set of recommendations, though there are new data available since their publication. All the guidelines reviewed place lithium and valproate at the top of the list of options for long-term treatment. There is a trend to increasingly recognize atypical antipsychotics, particularly olanzapine, as an additional alternative and an increasing prominence of lamotrigine for prevention of depressive relapses. All other treatment options currently have an extremely limited evidence base and do not feature consistently in the published guidelines.

Hsu FC, Garside MJ, Massey AE, McAllister-Williams RH. · Psychobiology Research Group, School of Neurology, Neurobiology and Psychiatry, University of Newcastle upon Tyne, Newcastle upon Tyne, UK. · Psychopharmacology (Berl). · Pubmed #12684731 No free full text.

Abstract: RATIONALE: Neuropsychological impairments seen in depression may be secondary to hypercortisolaemia. Repeated cortisol administration impairs episodic memory with an alteration in event-related potentials (ERPs) recorded during information retrieval. It is unclear whether such ERP effects are specific to episodic memory, or whether repeated cortisol administration is required. OBJECTIVE: To investigate the effect of a single dose of hydrocortisone on the neural correlates of episodic memory and error detection. METHODS: Twenty healthy subjects were treated with hydrocortisone (100 mg) or placebo orally, in a double-blind, two-way crossover study. ERPs were recorded during an episodic memory and a Stroop task, 1-3 h following the medication. RESULTS: Cortisol increased error rates during the Stroop task but had no effect on episodic memory. The magnitude of ERPs associated with incorrect response in the Stroop task between -250 ms and +500 ms post-response was increased by cortisol, with no effect on correct-response ERPs. There was no effect of cortisol on episodic memory-retrieval-dependent ERPs. CONCLUSIONS: Cortisol can impair not only episodic memory but also processes involved in error detection. In contrast to repeated cortisol administration, a single dose of cortisol does not alter the behavioural performance or the electrophysiological correlates of episodic memory. However, it increases error rates in a choice response task with associated quantitative changes in incorrect-response ERPs. This probably reflects an alteration in anterior cingulate cortex activity. Such changes may contribute to the neuropsychological impairment seen in depression. This study also demonstrates the utility of ERPs for investigating the effect of neuroendocrine manipulations on the neural correlates of neuropsychological function.

McAllister-Williams RH, Massey AE. · Psychobiology Research Group, School of Neurology, Neurobiology and Psychiatry, University of Newcastle, NE1 4LP, Newcastle upon Tyne, UK. · Psychopharmacology (Berl). · Pubmed #12589521 No free full text.

Abstract: RATIONALE: An involvement of 5-HT(1A) receptors is postulated in the pathophysiology of affective disorders and mechanism of action of antidepressants. Methods for studying their functional integrity in humans are, however, limited. Preliminary data suggests that activation of somatodendritic 5-HT(1A) receptors cause a negative shift in the EEG frequency spectrum. Animal research suggests that pindolol is an agonist at these receptors but an antagonist at postsynaptic 5-HT(1A) receptors. OBJECTIVE: We postulated that while pindolol would antagonise known postsynaptic mediated neuroendocrine responses to the 5-HT(1A) agonist buspirone, both drugs would have a similar effect on the EEG frequency spectrum. METHODS: Fourteen healthy men were administered placebo or pindolol (20 mg orally) 90 min before placebo or buspirone (30 mg orally) in a double blind cross-over study. Plasma prolactin and growth hormone were assayed and EEGs recorded before and after drug administration. RESULTS: A significant negative shift in the EEG frequency spectrum was found for both buspirone and pindolol, with the combination producing a similar effect to each drug alone. In contrast, the neuroendocrine response to buspirone was significantly attenuated by pindolol. CONCLUSIONS: The data obtained are consistent with the EEG effects of buspirone and pindolol being mediated by somatodendritic 5-HT(1A) receptors, in contrast to the neuroendocrine response, which is known to be mediated by postsynaptic receptors. The development of this novel method of assessing somatodendritic 5-HT(1A) receptors in humans is a potentially important advance which may allow the testing of hypotheses of its involvement in depression and response to antidepressants.

McAllister-Williams RH. · Institute of Neuroscience, Newcastle University, Newcastle upon Tyne NE1 4LP, UK. · Evid Based Ment Health. · Pubmed #18669671 No free full text.

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McMahon L, Foran KM, Forrest SD, Taylor ML, Ingram G, Rajwal M, Cornwall PL, McAllister-Williams RH. · Northumberland, Tyne and Wear NHS Trust, Sunderland. · Br J Gen Pract. · Pubmed #17976288 links to  free full text

Abstract: BACKGROUND: Based on data from large multicentre US trials, the National Institute for Health and Clinical Excellence (NICE) is advocating a stepped-care model for the management of depression, with 'case management' or 'collaborative care' for selected patients in primary care. AIM: To conduct a pilot study examining the use of graduate mental health workers case managing depressed primary care NHS patients. DESIGN OF STUDY: A randomised controlled trial comparing usual GP care with or without case management over 16 weeks of acute antidepressant drug treatment. SETTING: Three primary care practices in the North East of England. METHOD: Patients with depression, aged 18-65 years, who had failed to adequately respond to antidepressant treatment, were randomised to the two treatments. Assessments were made at baseline, 12, and 24 weeks using a combination of observer and self ratings. RESULTS: Randomisation of 62 patients required screening of 1073 potential patients. There was little difference in outcome between the two treatment arms but a gradual improvement in symptoms over time was seen. Client satisfaction was assessed as high across both treatments. CONCLUSION: While this pilot study confirmed the integrity of the study protocol and the suitability of the outcome measures and randomisation procedure, it raises questions regarding the practicality of recruitment and feasibility of the intervention. It would be crucial to address these issues prior to the implementation of a large multi-centre randomised controlled trial.

Alhaj HA, Massey AE, McAllister-Williams RH. · Psychobiology Research Group, School of Neurology, Neurobiology and Psychiatry, University of Newcastle upon Tyne, Leazes Wing, Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP, United Kingdom. · J Psychiatr Res. · Pubmed #17054990 No free full text.

Abstract: Altered laterality of cortical activity, neuropsychological impairment and hypercortisolaemia have been shown in depression. The neural correlates of episodic memory in healthy subjects demonstrate hemispheric laterality but it is not known whether this is affected by depression and/or hypercortisolaemia. Twenty-seven drug-free depressed patients and 29 matched healthy controls were studied. Event-related potentials (ERPs) were recorded during an episodic memory test. During the study phase, subjects heard words spoken in either a male or female voice. Old and new words were presented visually during a test phase, when subjects were requested to identify words as old or new and recollect the gender of the voice for old words. Cortisol levels were measured in saliva and plasma samples. The results showed a trend for elevated salivary cortisol concentration in depressed patients. Reaction times were significantly longer in patients; however, there was no difference in memory accuracy performance between the two groups. Recollection performance was found to be negatively correlated with age, with a similar trend for cortisol concentrations. ERP activity not specifically related to episodic memory retrieval recorded 200-500ms post-stimulus from controls showed a marked laterality, with higher voltages over the right hemisphere; however, was not seen in patients. There was significant correlation between cortisol and the laterality of the neural activity specifically related to episodic memory retrieval recorded 500-1400ms post-stimulus in both depressed and healthy groups. These unique findings demonstrate that while the laterality of the neural correlates of episodic memory is sensitive to cortisol, it is not altered by the non-specific laterality effects seen in depression.

Wiśniewski GS, McAllister-Williams RH, Jakitowicz J, Nowicki Z, Majkowicz M, Trzebiatowska IA. · No affiliation provided · Biol Psychiatry. · Pubmed #18801473 No free full text.

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McAllister-Williams RH, Foran K, Forrest S, Ingram G, McMahon L, Taylor M, Rajwal MS, Cornwall PL. · No affiliation provided · J Psychopharmacol. · Pubmed #17060347 No free full text.

This publication has no abstract.

McAllister-Williams RH, Foran K, Forrest S, Ingram G, McMahon L, Taylor M, Rajwal M, Cornwall L. · No affiliation provided · Br J Gen Pract. · Pubmed #17007717 links to  free full text

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McAllister-Williams RH, Young AH, Menkes DB. · No affiliation provided · Br J Psychiatry. · Pubmed #10789339 links to  free full text

This publication has no abstract.