The objective of this study was to assess the effectiveness and tolerability of galantamine in patients with mild-to-moderate Alzheimer's disease (AD) in everyday clinical practice. Patient selection was made on 36 sequential patients attending Belfast City Hospital Memory Clinic between December 2000 and June 2001. Patients were treated with galantamine for 6 months, starting from 4 mg twice daily increasing to 8 mg twice daily and then to 12 mg twice daily at 4-weekly intervals. Patients (25 females, 11 males), mean age 78 years (59–90), were diagnosed with probable AD and had a mini-mental state examination (MMSE) score of 10–26. Efficacy was assessed using the MMSE, neuropsychiatric inventory (NPI), neuropsychiatric inventory caregiver distress (NPI-D) scale and the Bristol activities of daily living (B-ADL) scale at baseline and after 3 and 6 months of treatment. Mean improvements were noted on all four measures of efficacy at 3 and 6 months; improvements were significant on the MMSE, NPI and NPI-D at 3 months and on the NPI-D at 6 months. Galantamine was overall well tolerated. The most common adverse events were gastrointestinal, particularly nausea. Four patients stopped treatment due to adverse events, and seven were stabilised on 8 mg twice daily as they were unable to tolerate the target dose. This naturalistic study confirms clinical trial data, which shows galantamine improves cognition and behavioural symptoms and is overall well tolerated.
A survey of dependency levels was carried out in 1985 and 1989 in 41 residents of old peoples homes and 25 patients in geriatric continuing care wards. There was an increase in all levels of dependency for those in both types of care. In the hospital patients surveyed in 1985, mortality was greatest in the most dependent, particularly those with impaired mental function. There was a positive correlation between length of survival and mental function. The results of this study emphasise the important role of dementia in the health and survival of old people.
Hyperglycaemia has been observed after acute stroke, and is associated with a poor prognosis. It is not known whether this is due to the stress response of the acute illness or whether hyperglycaemia is, in itself, harmful to ischaemic nervous tissue. Seventy-one patients admitted to hospital with acute stroke and no history of diabetes or other acute illness were recruited, and fasting blood sampling was carried out within 24 h of symptom onset, for plasma glucose and stress hormones and levels of haemoglobin A1c (HbA1c). Computerized tomography of the brain was carried out on 77% of the subjects. The subjects were followed up for 3 months or until death. Glucose levels were higher in subjects who died during the course of the study (p = 0.025), but this relationship became non-significant after age (p < 0.001) and cortisol (p = 0.001) levels were taken into account with multivariate analysis. The correlation between serum cortisol and the volume of the lesion on CT scan was also stronger than the relation of glucose with volume. Haemoglobin A1c had no relationship with either mortality or lesion volume. These findings suggest that the hyperglycaemia seen after an acute stroke is secondary to a stress response and they do not support the theory of hyperglycaemia being harmful to ischaemic nervous tissue. These findings have implications for the treatment of acute stroke with hypoglycaemic agents.
an increase in mean platelet volume and a decrease in platelet total have been reported following stroke and increased mean platelet volume in acute myocardial infarction has been shown to be predictive of mortality.given the established seasonal variation in morbidity and mortality from cardiovascular disease and various risk factors for the disease, we explored the seasonal variation in mean platelet volume and platelet total.we assessed levels of platelet count, platelet volume, fibrinogen, factor VII, core body and ambient temperatures in 54 healthy community dwelling elderly volunteers over a period of 1 year. We used cosinor rhythmometry to quantify and compare the seasonal rhythms.we found significant seasonal variation in fibrinogen, mean platelet volume and core body temperature all of which peaked synchronously in May/June, in a year with an atypically mild winter and hot summer. Platelet total and factor VII did not exhibit a seasonal rhythm.we conclude that the synchrony between peak size of platelets and peak level of fibrinogen will significantly increase the likelihood of thrombotic events. These results provide further evidence of a seasonal pro-thrombotic state, which has a complex relationship with temperature.
To test the hypothesis that higher levels of fibrinogen in winter are related to infections via the acute phase response, we assessed seasonal variation in fibrinogen and C‐reactive protein, together with three other responses to infection: white cell count, human herpesvirus‐6 IgG antibody and interleukin‐6. Monthly blood samples from 24 subjects aged 75+ years were assessed for fibrinogen, C‐reactive protein, white cell count, and human herpesvirus‐6 IgG antibody. Interleukin‐6 was measured in seven. Seasonal variation of these measures was determined by the population‐mean cosinor procedure. Fibrinogen had a significant seasonal variation with a winter peak (mid‐February) 1.26 g/l above the corresponding summer trough. C‐reactive protein had a late‐February peak, 3.71 mg/l above the summer trough. No seasonal rhythm was found in any other response to infection investigated. This study provides no evidence that winter infections are responsible for the seasonal variation in fibrinogen or C‐reactive protein. The explanation for the seasonal changes in these proteins remains unknown.
Patients are often referred to osteoporosis clinics with a radiological diagnosis of osteoporosis. Previous studies attempting to ascertain risk of osteoporosis from radiographs have been conflicting. The aim of our study was to determine how reliable spinal radiographs were at detecting low bone density compared with Dual Energy X ray Absorptiometry (DXA). We retrospectively measured the Bone Mineral Density (BMD) at the spine in 130 patients with a radiological diagnosis of osteopenia or osteoporosis in the absence of vertebral fractures. They were compared with a group of 119 age and sex matched patients with one or more low trauma vertebral fractures. There was a statistically significant difference in the mean BMD between these two groups. 12.7%, of the x-ray group with osteopenia reported, had a normal bone density, 49.2% had osteopenia (T-score -1 to -2.5) and 38.1% had osteoporosis (T-score <-2.5). Of those with a radiological report of osteoporosis, 12.8% had a normal bone density, 44.7% had osteopenia and 42.6% had osteoporosis. We conclude that a radiological report of low bone density is a strong predictor of osteopenia or osteoporosis by BMD measurement.
A clinical audit of ward practice for diagnosing and treating urinary tract infection was carried out to assess the impact on clinical practice four years after publication of a working protocol. Data were collected from all medical, surgical, gynaecology and geriatric wards in 25 hospitals in Northern Ireland. All wards made use of urinary dipsticks for ward testing, as recommended by the protocol. However many negative samples were still forwarded for laboratory analysis. The potential financial savings which would result from effective ward screening were not being realised and the publication appeared to have minimal impact on clinical practice. Advice on an improved diagnostic protocol for urinary tract infection may not have been disseminated to the nursing staff whose role was pivotal in the screening process.
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