Implementation of CAGE alcohol screening in a primary care practice.

BACKGROUND AND OBJECTIVES: Alcoholism is a common problem in primary care. Although the four-question CAGE screening tool was developed for use by primary care physicians, studies show that the questionnaire is still not widely used in clinical practice. This study tested the effectiveness of an intervention to increase physicians' use of the CAGE questions. METHODS: We reviewed medical records charts completed by 15 family practice residents for documented alcoholism screening, both before and after an educational intervention. The intervention included modification of examination forms to include the CAGE questions, as well as written feedback from faculty members regarding residents' documentation of alcohol screening. RESULTS: We reviewed a total of 170 pre- and 227 post-intervention charts. Following educational intervention, documentation of quantity/frequency of alcohol beverage consumption increased from 26.5% to 93%. The use of CAGE screening increased from 5.9% to 76.7%. For post-intervention charts that documented using the four CAGE questions, 12.6% showed one or more positive responses. Of these charts, 27% documented physician intervention such as a warning or referral for treatment of alcohol-related problems. CONCLUSIONS: Our educational intervention was a successful way to improve physicians' use of CAGE questions to screen for alcoholism.

Neurovascular permeability and fibrin deposition in the central neuraxis of Lewis rats with cell-transferred experimental allergic encephalomyelitis in relationship to clinical and histopathological features of the disease.

Abrupt increases in blood-brain barrier (BBB) permeability were detected by the dual-isotope technique, coinciding with evidence of activation of coagulation cascade, occurred 1 day prior to appearance of clinical neurological signs of experimental allergic encephalomyelitis (EAE) and in conjunction with initial detectable cell infiltration. Maximal increase of BBB permeability was observed on the first day of clinical signs, which was 2 days prior to maximum severity of clinical abnormalities and 1 day in advance of the greatest number of central nervous system (CNS) fibrin deposits and perivascular cellular infiltration. Returning of increased BBB permeability and CNS perivascular fibrin deposits to normal levels was demonstrated prior to complete remission of neurological signs. Considerable CNS perivascular cellular infiltrates, however, lasted after complete remission of neurological signs. These findings indicate that increased permeability of the BBB, in association with activation of the coagulation cascade, is the earliest expressions of immune effector activity of experimental allergic EAE.

Concordance and localization of maximal vascular permeability change and fibrin deposition in the central neuraxis of Lewis rats with cell-transferred experimental allergic encephalomyelitis.

This study utilized Lewis rats and the cell-transfer form of experimental allergic encephalomyelitis (EAE) to focus on two central nervous system microvascular alterations known to be intimately associated with early clinical neurological signs of the disease, namely increased vascular permeability and deposition of fibrin. The main objective of the work was to define the degree of concordance and the anatomical localization of maximal vascular permeability change and fibrin deposition within the neuraxis of recipient rats during the earliest expression of clinical manifestations of the disease. Recipients were injected with predetermined doses of activated, myelin basic protein (MBP)-reactive syngeneic donor lymphoid cells and killed 6 or 7 days later when they exhibited the first clinical signs of disease. This experimental design allowed assessment of late occurring immune activities of a single population of MBP-reactive effector cells. Increased vascular permeability, expressed as mean extravascular blood equivalents (EVBE), attained maximum change, i.e., 16.04 +/- 5.07, within the lumbosacrococcygeal segment of the spinal cord (LSC). Maximal density of fibrin depositions, i.e., 192 +/- 94 deposits, also occurred within the LSC cord. The concordance of these two histoimmunopathological events, their tight linkage to early clinical signs of disease and the fact that both events attained maximal values within the LSC cord suggest that increased permeability and activation of the coagulation cascade may be prerequisite events for the expression of neurological signs of EAE.