Is the Epworth sleepiness scale suitable for use in stroke?

BACKGROUND: The Epworth Sleepiness Scale (ESS-8) is frequently used in stroke but has never been validated for this condition. There is concern regarding the suitability of the driving item (item 8). A summed raw score of 10 or more (from a maximum of 24) signifies pathological sleepiness. OBJECTIVE: To determine the construct validity of the ESS-8 by Rasch analysis and in particular to determine whether omission of item 8 confounds the scale. METHOD: A pack containing the ESS-8 and questions regarding sleep and demographics was sent to 999 patients who had experienced a stroke within the past 4 years. Data were assessed for fit to the Rasch model. RESULTS: Analysis of 269 records revealed a unidimensional scale that was free from differential item functioning by age and sex with good overall fit to the Rasch model. Item 4 had disordered thresholds. Analysis of the ESS without item 8 (ESS-7) also revealed a valid scale. Equating person locations between the ESS-8 and ESS-7 showed no differences below a summed raw score of 18. CONCLUSION: The ESS-8 has good construct validity for use in stroke and is reliable at the cutpoint of 10. Summed raw scores below 18 will be unaffected if nondrivers either score as zero or simply omit item 8. The scale is therefore robust for detecting cases of pathological sleepiness in stroke but may not be suitable for measuring high levels of sleepiness in a sample containing both drivers and nondrivers. Instead, the ESS-7 could be used for this purpose.

Effects of hormone replacement therapy on the phospholipid composition of high density lipoproteins in postmenopausal women.

The beneficial effect of hormone replacement therapy (HRT) in reducing the risk of cardiovascular disease may be partly mediated by favourable changes in the phospholipid composition of high density lipoprotein (HDL) subclasses. In group A(oestrogen alone) HDL phosphatidylcholine increased (P<0.01), while 2 there was a decrease in HDL phosphaditylinositol (P<0.05) 2 and HDL phosphatidylethanolamine (P<0.01) compared with 2 controls (baseline). In the same group, HDL phosphatidylcholine 3 increased (P<0.01) and HDL phosphatidylethanolamine decreased (P<0.05). In group B (oestrogen plus progestogens), HDL phosphatidylcholine increased (P<0.001) while there were 2 decreases in HDL sphingomyelin (P<0.01), HDL 2 2 phosphatidylserine (P<0.05), HDL phosphatidylethanolamine 2 (P<0.01) and HDL diphosphatidylglycerol (P<0.05). In the 2 same group, an increase in HDL phosphatidylcholine (P<0.01) 3 and HDL phosphatidylserine (P<0.01) were observed, as well 3 as a decrease in HDL phosphatidylethanolamine (P<0.001). 3 The significance of these results is discussed.

Diazepam treatment in rats induces changes in the concentrations of different phospholipid classes in liver and liver mitochondria.

Liver phospholipid concentrations were determined in rats after the administration of diazepam (5 mg/Kg/day), for a period of two months. Increased concentrations of total phospholipids (P < 0.05), phosphatidylcholine (P < 0.05) and phosphatidylinositol (P < 0.05) were found in the rats taking diazepam. In contrast, a decreased concentration of phosphatidylserine (P < 0.01) was observed in the same group of animals. In addition, changes in the concentration of rat liver mitochondrial phospholipids after the administration of diazepam during the same period of time were determined. Increased concentrations of total phospholipids (P < 0.01), phosphatidylcholine (P < 0.001) and diphosphatidylglycerol (P < 0.001) were found in the rats treated with diazepam. In contrast, decreased phosphatidylserine (P < 0.001) and phosphatidylinositol (P < 0.01) concentrations were observed in the same group of animals. The considerable changes observed in liver phospholipids and individual classes of liver mitochondrial phospholipids induced by long-term administration of diazepam, possibly suggest a stimulation of liver phospholipid biosynthesis. This effect may be related to enzymatic systems which are involved in phospholipid pathways, and are linked to benzodiazepinergic binding sites.