Elizabeth M. Scott
University of Sydney
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Featured researches published by Elizabeth M. Scott.
Biological Psychiatry | 1995
Ian B. Hickie; Elizabeth M. Scott; Philip B. Mitchell; Kay Wilhelm; Marie-Paule Austin; Barbara Bennett
In 39 hospital inpatients with severe primary depressive disorders, we evaluated the relationships between subcortical hyperintensities on magnetic resonance imaging (MRI) and clinical features, neuropsychological impairment and response to standard therapies. Both white matter and gray nuclei lesions were associated with older age and the absence of a family history of affective disorder. White matter hyperintensities were also associated with onset of first affective episode after the age of 50 years and impaired psychomotor speed. Most importantly, the severity of white matter hyperintensities predicted a poorer response to treatment (r = -0.44, p < .01). Negative correlations of the same order were detected in those (n = 20) who received electroconvulsive therapy (r = -0.42, p = .06) and those (n = 19) who received pharmacotherapy alone (r = -.49, p < .05). This study provides preliminary evidence supporting the clinical and prognostic significance of extensive white matter hyperintensities in patients with severe depression.
Psychological Medicine | 2001
Ian B. Hickie; Elizabeth M. Scott; Sharon L. Naismith; Philip B. Ward; Keelin Turner; Gordon Parker; Philip B. Mitchell; Kay Wilhelm
BACKGROUND Neuropsychiatric research needs to examine the relationships between aetiological, genotypic and clinical risk factors and behavioural phenotypes. These relationships can now be examined in older patients with depressive disorders. METHODS Key behavioural features, clinical and vascular risk factors and putative genotypes for late-onset neurodegenerative disorders and/or vascular disease were recorded in 78 older patients with depression (mean age = 549 years, S.D. = 14.1) and 22 healthy control subjects (mean age = 55.5 years, S.D. = 9.6). RESULTS Two or more vascular risks were more common in older patients (65% v. 26% of control subjects, P < 0.01), and in patients with late-onset disorders (82% v. 57% in patients with early-onset disorders, P < 0.05). Patients with late-onset depression had a higher prevalence of the homozygous or heterozygous forms of the C677T mutation of the methylenetetrahydrofolate reductase enzyme (MTHFR)(74% v. 48% in patients with early-onset disorders, P < 0.05). In a multivariate model, only presence of the MTHFR gene mutation predicted late-onset depression (odds ratio = 3.8, 95% CI = 1.1-12.9). Neither apolipoprotein E epsilon 4 or epsilon 2 was associated with depression, late-onset depression, cognitive impairment, or psychomotor change. Patients with apolipoprotein E epsilon 4 were less likely to have psychotic forms of depression. CONCLUSIONS Patients with late-onset depression had an increased rate of the C677T MTHFR gene mutation and other vascular risk factors. This suggests that a proportion of these patients may have genetically-determined and/or other vascular aetiologies. Patients at risk of these disorders may be assisted by currently-available preventative strategies.
Journal of Affective Disorders | 2013
Rébecca Robillard; Sharon L. Naismith; Naomi L. Rogers; Tony K.C. Ip; Daniel F. Hermens; Elizabeth M. Scott; Ian B. Hickie
BACKGROUND Circadian disturbances may play a key role in the pathogenesis of some forms of mood disorders. Despite marked changes in circadian rhythms during the normal course of adolescence and young adulthood, less is known about changes in the 24-h sleep-wake cycle in young persons with mood disorders. METHODS Seventy-five young participants with mood disorders (unipolar: n=46, 20.1 ± 4.7 years old; bipolar I or II: n=29, 23.2 ± 4.3) and 20 healthy participants (24.8 ± 2.5 years old) underwent actigraphy monitoring during a depressive phase over seven consecutive days and nights. Sleep phase delay was defined as mean sleep onset ≥ 1:30 am and/or sleep offset ≥ 1 0:00 am. RESULTS A delayed sleep phase was found in 62% of participants with bipolar disorders when depressed, compared with 30% of those with unipolar depression (χ(2)=6.0, p=0.014) and 10% of control participants (χ(2)=11.2, p<0.001). Sleep offset times were significantly later in subjects with mood disorders compared to the control group, and later in those with bipolar as compared with unipolar disorders (all p ≤ 0.043). LIMITATIONS This study was cross-sectional and the depressed groups were somewhat younger compared to the healthy controls. Longitudinal studies are required to determine the predictive significance of these findings. CONCLUSIONS Young patients with mood disorders, especially those with bipolar disorders, are particularly likely to have a delayed sleep phase. Therapies focused on advancing sleep phase may be of specific benefit to these young persons.
The Medical Journal of Australia | 2012
Elizabeth M. Scott; Daniel F. Hermens; Nick Glozier; Sharon L. Naismith; Adam J. Guastella; Ian B. Hickie
Objective: To assess the extent to which youth‐specific, mental health care centres engage young people (12–25 years of age) in treatment, and to report the degree of psychological distress, and the diagnostic type, stage of illness, and psychosocial and vocational impairment evident in these young people.
Journal of Affective Disorders | 2010
Sharon L. Naismith; M. Antoinette Redoblado-Hodge; Simon J.G. Lewis; Elizabeth M. Scott; Ian B. Hickie
BACKGROUND Neuropsychological deficits in depression include difficulties with psychomotor speed, executive functions and memory. Some of these changes persist despite antidepressant treatment. While research in other areas of psychiatry has shown cognitive training techniques to be effective, only one study has evaluated this approach in depression. METHODS Sixteen patients (mean age=33.5years) with a lifetime diagnosis of major depressive disorder were administered a standardised battery of neuropsychological tests and allocated to treatment (n=8) or waitlist control (n=8) conditions. The treatment consisted of 10-weeks of twice weekly cognitive training using the Neuropsychological Educational Approach to Remediation. All participants were re-assessed after 10-weeks by interviewers blinded to group allocation. RESULTS Participants in the treatment condition demonstrated greater improvements on tests of memory encoding and memory retention than the waitlist control group. There were no observable benefits in terms of psychomotor speed or executive functions or in self-reported levels of disability. Affective symptoms also remained stable. LIMITATIONS This study included a small sample of participants and treatment allocation was not randomised. CONCLUSIONS Cognitive training in affective disorders improves memory performance. It may be an effective non-pharmacological treatment option for improving cognitive functions, which in turn, may improve psychosocial functioning and reduce disability. This study supports theories suggesting cognitive training may promote neuroplasticity.
Australasian Psychiatry | 1998
Ian B. Hickie; Dusan Hadzi-Pavlovic; Elizabeth M. Scott; Tracey A. Davenport; Annette Koschera; Sharon L. Naismith
Although 18% of Australians suffered a psychiatric disorder in the last 12 months, only 38% presented to health services. Of these, the vast majority (76%) consulted their general practitioner [1]. While two-thirds of those who present to primary care have significant psychological symptoms, at least 30% have psychological disorders that result in disability, long-term morbidity and/or mortality [2–4]. These disorders are often co-morbid with other medical disorders and/or substance abuse [1]. Despite the advances in pharmacological and non-pharmacological therapies available [5,6] less than half of the patients who present receive a psychiatric diagnosis and less than half of these receive any specific treatment [7]. Recommendations under the National Mental Health Strategy [8] recognise the urgent need for educational programs and practice support mechanisms to correct these major public health deficits.
Psychological Medicine | 1998
Ian B. Hickie; Elizabeth M. Scott
The severe depressive disorders of late life are associated with high rates of medical morbidity and mortality, cognitive impairment, suicide, disability, complex treatment regimens, institutionalization and high costs to the community (Murphy, 1983; Murphy et al. 1988; Bruce & Leaf, 1989; NIH Consensus Development Panel, 1992; Alexopoulos et al. 1993a, b ; Brodaty et al. 1993; Bruce et al. 1994; Forsell et al. 1994; Hickie et al. 1995; Blazer, 1996). Those disorders that are accompanied by cognitive impairment and}or concurrent medical morbidity have a particularly poor outcome (Bruce & Leaf, 1989; Alexopoulos et al. 1993b ; Hickie et al. 1995, 1997a). Although psychosocial models of late-life depression place considerable importance on age-related psychological and social risk factors, those who survive into later life may actually be characterized by psychological resilience (Henderson, 1994; Blazer, 1997). Current aetiological research in late-life depression, therefore, places particular emphasis on the potential role of biological risk factors. The potential importance of vascular risk factors is receiving renewed attention and may provide opportunities for specific prevention and intervention strategies in high-risk populations. This emphasis on possible vascular risk factors, and the wider importance of vascular pathologies in late-life neuropsychiatric disorders, mirrors the emphasis of much earlier clinico-pathological studies (Binswanger, 1894; Alzheimer, 1895). The specific focus on the importance of small progressive changes within the subcortical white matter, as distinct from more discrete cortical infarcts (Olszewski, 1962), is now supported by the emerging neuroimaging literature and theoretical constructs in late-life depression (Krishnan, 1991, 1993; Hickie et al. 1996, 1997b ; Krishnan et al. 1997).
Australasian Psychiatry | 2009
Elizabeth M. Scott; Sharon L. Naismith; Bradley Whitwell; Blake Hamilton; Catherine Chudleigh; Ian B. Hickie
Objective: Evidence suggests that quality mental health care is based on well-integrated multi-disciplinary care provided by a range of mental health, substance use, and general healthcare clinicians. There is a growing focus in Australia on providing this type of mental health care to young people, particularly those in the early stages of a major disorder. The development of such services has proceeded on the basis of limited service-based data and has also been impeded by current healthcare funding structures. Methods: This report outlines the service characteristics of three models: a traditional ‘fee for service’ model, a specialized youth mental health clinic, and a new headspace multi-disciplinary site in South Western Sydney. Results: Naturalistic data from these three services collected during their developmental phase indicate that each model is associated with differential demographic, illness and service organization characteristics. Conclusions: Compared with ‘fee-for-service’ type care, specialized youth models provide greater access to a broad range of multi-disciplinary clinicians.
Early Intervention in Psychiatry | 2013
Ian B. Hickie; Elizabeth M. Scott; Daniel F. Hermens; Sharon L. Naismith; Adam J. Guastella; Manreena Kaur; Anna Sidis; Bradley Whitwell; Nick Glozier; Tracey A. Davenport; Christos Pantelis; Stephen J. Wood; Patrick D. McGorry
Aim: The study aims to apply clinical staging to young people who present for mental health care; to describe the demographic features, patterns of psychological symptoms, disability correlates and clinical stages of those young people; and to report longitudinal estimates of progression from less to more severe stages.
European Psychiatry | 2013
Rébecca Robillard; Sharon L. Naismith; Naomi L. Rogers; Elizabeth M. Scott; T.K.C. Ip; Daniel F. Hermens; Ian B. Hickie
This study evaluated the potential of circadian measures as early markers of mood disorders subtypes. Patients with bipolar disorders had significantly lower levels and later onset of melatonin secretion than those with unipolar depression. Furthermore, abnormal phase angles between sleep, melatonin and temperature were found in several patients.