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E Jane Byrne

Publications and source records attributed to E Jane Byrne.

5 recordsLinked to original sources
PubMed2007

The role of vascular risk factors in late onset bipolar disorder.

BACKGROUND: The association between late life depression and cerebro-vascular risk and cerebro-vascular disease is well established. Do similar links exist with late onset bipolar disorder? AIMS AND OBJECTIVES: Patients with early onset (less than 60 years of age) bipolar disorder were compared with those of late onset (aged 60 and above) in relation to cognitive function, physical health and vascular risk factors. METHOD: Cross-sectional survey of elderly bipolar disorder patients (above 65 years) involved with secondary care mental health services. Thirty patients with early onset were compared with 20 patients with a late onset bipolar disorder. Diagnosis of bipolar disorder was according to ICD-10 criteria and without an associated clinical diagnosis of dementia. Assessment of cognition included tests of frontal-executive function, and cerebro-vascular risk was quantified with the Framingham stroke risk score. RESULTS: The late onset group had a higher stroke risk score than the early onset group, this difference persisting despite taking age and gender differences into account. However, late onset patients' cognitive function (including frontal lobe tests) and physical health status was no different to the early onset group. CONCLUSION: There is higher 'cerebrovascular risk' in elderly patients with late onset bipolar disorder, compared to patients with an early onset. This suggests that cerebrovascular risk may be an important factor for the expression of bipolar disorders in later life, and has significant management implications for older bipolar patients.

Adult↗
PubMed2005

Grouping for behavioral and psychological symptoms in dementia: clinical and biological aspects. Consensus paper of the European Alzheimer disease consortium.

Behavioral and psychological symptoms of dementia (BPSD), constitute a major clinical component of Alzheimer's disease (AD). There is a growing interest in BPSD as they are responsible for a large share of the suffering of patients and caregivers, and they strongly determine the patient's lifestyle and management. Better detection and understanding of these symptoms is essential to provide appropriate management. This article is a consensus produced by the behavioral group of the European Alzheimer's Disease Consortium (EADC). The aim of this article is to present clinical description and biological correlates of the major behavioral and psychological symptomatology in AD. BPSD is not a unitary concept. Instead, it should be divided into several symptoms or more likely: groups of symptoms, each possibly reflecting a different prevalence, course over time, biological correlate and psychosocial determinants. There is some clinical evidence for clusters within groups of BPSD. Biological studies indicate that patients with AD and BPSD are associated with variations in the pathological features (atrophy, brain perfusion/metabolism, histopathology) when compared to people with AD without BPSD. An individually tailored approach taking all these aspects into account is warranted as it may offer more, and better, pharmacological and non-pharmacological treatment opportunities.

Aged↗
PubMed2004

Rivastigmine for dementia associated with Parkinson's disease.

BACKGROUND: Cholinergic deficits are prominent in patients who have dementia associated with Parkinson's disease. We investigated the effects of the dual cholinesterase inhibitor rivastigmine in such patients. METHODS: Patients in whom mild-to-moderate dementia developed at least 2 years after they received a clinical diagnosis of Parkinson's disease were randomly assigned to receive placebo or 3 to 12 mg of rivastigmine per day for 24 weeks. Primary efficacy variables were the scores for the cognitive subscale of the Alzheimer's Disease Assessment Scale (ADAS-cog) and Alzheimer's Disease Cooperative Study-Clinician's Global Impression of Change (ADCS-CGIC). Secondary clinical outcomes were the scores for the Alzheimer's Disease Cooperative Study-Activities of Daily Living, the 10-item Neuropsychiatric Inventory, the Mini-Mental State Examination, Cognitive Drug Research power of attention tests, the Verbal Fluency test, and the Ten Point Clock-Drawing test. RESULTS: A total of 541 patients were enrolled, and 410 completed the study. The outcomes were better among patients treated with rivastigmine than among those who received placebo; however, the differences between these two groups were moderate and similar to those reported in trials of rivastigmine for Alzheimer's disease. Rivastigmine-treated patients had a mean improvement of 2.1 points in the score for the 70-point ADAS-cog, from a baseline score of 23.8, as compared with a 0.7-point worsening in the placebo group, from a baseline score of 24.3 (P<0.001). Clinically meaningful improvements in the scores for the ADCS-CGIC were observed in 19.8 percent of patients in the rivastigmine group and 14.5 percent of those in the placebo group, and clinically meaningful worsening was observed in 13.0 percent and 23.1 percent, respectively (mean score at 24 weeks, 3.8 and 4.3, respectively; P=0.007). Significantly better outcomes were seen with rivastigmine with respect to all secondary efficacy variables. The most frequent adverse events were nausea (affecting 29.0 percent of patients in the rivastigmine group and 11.2 percent of those in the placebo group, P<0.001), vomiting (16.6 and 1.7 percent, P<0.001), and tremor (10.2 and 3.9 percent, P=0.01). CONCLUSIONS: In this placebo-controlled study, rivastigmine was associated with moderate improvements in dementia associated with Parkinson's disease but also with higher rates of nausea, vomiting, and tremor.

Aged↗