Use of physostigmine in the management of gamma-hydroxybutyrate overdose.
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Biomedical subjects
Publications and source records attributed to L Quang.
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OBJECTIVE: Since little is known concerning factors which may influence long-term prognosis of patients presenting with lacunar stroke, we conducted a longitudinal study of this stroke subtype. Variables likely to affect outcome were assessed at baseline, including those from transoesophageal echocardiographic studies. METHODS: Consecutive patients presenting with first-ever lacunar stroke underwent diagnostic workup that included brain CT or MRI, carotid duplex, and transthoracic and transoesophageal echocardiography. An assessment of patients was planned at entry (baseline), and thereafter every 12 months (clinic visit or telephone call), drop-out, or endpoint. The primary endpoint was nonfatal or fatal stroke. Secondary endpoint was death due to any cause. RESULTS: Among 60 consecutive lacunar patients with the mean follow-up period of 3.9 years, 12 patients (20%) had stroke recurrence. The mean annual rate for stroke was 5.2%, and for death 2.8%. For multivariate Cox proportional hazards analysis, the following three variables with the values of p < 0.1 after univariate testing were chosen: age (p = 0.095); aortic atheroma (p = 0.066); and any source of embolism from heart (p = 0.007). Any source of embolism from heart was the only factor which significantly enhanced the risk of stroke recurrence (p = 0.015). Using Kaplan-Meier life table analysis, the curves of percent free of recurrent stroke were significantly different (log rank test p = 0.002). CONCLUSIONS: Until the mechanism of lacunar stroke is better understood, it is reasonable to suggest that its investigation and prevention should be directed at all potential causes of future strokes including cardioembolism.
To reassess the independent risk factors for lacunar stroke and to clarify the role of potential embolic sources, we conducted a case-control study using transesophageal echocardiography and duplex ultrasonography. Among 62 consecutive patients with their first lacunar stroke and 202 normal controls, we found that hypertension (p < 0.001), smoking (p = 0.001), and aortic arch atheroma (p = 0.006) were independently associated with an increased risk of lacunar stroke. Whether proximal aortic arch atheroma is mechanistically associated with lacunar stroke or merely coexistent is uncertain.
STUDY OBJECTIVES: To estimate the cost per woman participating in a mammographic screening programme, and to describe methods for measuring costs. DESIGN: Expenditure, resource usage, and throughput were monitored over a 12 month period. Unit costs for each phase of the screening process were estimated and linked with the probabilities of each screening outcome to obtain the cost per woman screened and the cost per breast cancer detected. SETTING: A pilot, population based Australian programme offering free two-view mammographic screening. PARTICIPANTS: A total of 5986 women aged 50-69 years who lived in the target area, were listed on the electoral roll, had no previous breast cancer, and attended the programme. RESULTS: Unit costs for recruitment, screening, and recall mammography were $17.54, $60.04, and $175.54, respectively. The costs of clinical assessment for women with subsequent clear, benign, malignant (palpable), and malignant (impalpable) diagnoses were $173.71, $527.29, $436.62, and $567.22, respectively. The cost per woman screened was $117.70, and the cost per breast cancer detected was $11,550. CONCLUSIONS: The cost per woman screened is a key variable in assessment of the cost effectiveness of mammographic screening, and is likely to vary between health care settings. Its measurement is justified if decisions about health care services are to be based on cost effectiveness criteria.
Smoking is now a well established risk factor for ischaemic stroke. However, the risk associated with smoking may differ between subgroups of ischaemic stroke. To test the hypothesis that cortical ischaemia due to carotid artery occlusive disease, the latter of which has previously been linked to smoking, may have a higher smoking risk compared to other forms of cerebral ischaemia, we identified 178 cases of cortical ischaemia presumably due to carotid occlusive disease in our previous case-control population and compared the odds ratios (OR) for smoking risk in this group with that in group of 244 cases of other forms of cerebral ischaemia combined. All cases were individually matched for age (+/- 5 years) and sex with neighbourhood controls. Multiple conditional logistic regression was used to adjust for potentially confounding factors. The OR for current smokers in the cortical group was higher than that in the non-cortical group [OR 4.4, 95% confidence interval 2.2, 8.9 vs. 2.1 (1.1, 4.1)], particularly for those who smoked more than 60 pack-years [5.5 (2.2, 14.0) vs. 1.5 (0.6, 3.8)] and those who currently smoked more than one pack per day [20.2 (3.3, 122.3) vs. 2.6 (0.8, 8.2)], but not significantly. Overall, there is some evidence to suggest that smoking may be a more potent risk factor for cortical than for other forms of cerebral ischaemia, particularly at high smoking rates. Further studies are needed to substantiate this finding.
Transient ischemic attacks (TIAs) are not homogeneous and may consist of subsets with mechanisms as varied as their stroke counterparts. We describe a form of TIA in 50 patients where crescendo episodes of ischemia were restricted to the region of the internal capsule, usually causing symptoms affecting face, arm, and leg. These patients composed 4.5% of a consecutive series of patients admitted with TIAs over a 15-year period and 33% of all TIAs classified as subcortical. We believe that the ischemia was most often due to hemodynamic phenomena in diseases, single, small penetrating vessels. When cerebral infarction developed, it was usually lacunar and involved a single penetrating vessel, although occasionally striatocapsular or anterior choroidal artery territory infarction occurred. There was no evidence of artery-to-artery or heart-to-artery embolism. Resistance to various forms of therapy, including hemodiluting, anticoagulant, and thrombolytic agents, was common. Because of dramatic and easily recognizable clinical presentation, apparent specific pathophysiologic mechanism, and the development of early capsular stroke in a high proportion of cases (42%), we have termed this the "capsular warning syndrome."
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