The Community Screening Interview for Dementia "CSI {D|# was developed as a screening instrument for dementia for use in cross!cultural studies[ It consists of two components\ a cognitive test for non!literate and literate populations and an informant interview regarding performance in everyday living[ The development of the CSI {D|\ involving harmonization\ translation\ back translation and pilot testing\ for use in _ve sites is described[ The results demonstrate the adaptability and utility of the CSI {D| in populations from very di}erent socioeconomic backgrounds[ The inclusion of informant data adds signi_cantly to the performance of the CSI {D| as a dementia screen[ The combination of informant and cognitive scores in a discriminant score produces better sensitivity and speci_city for dementia than cognitive scores alone[ The informant score has a signi_cant independent e}ect in predicting dementia[ Copyright Þ 1999 John Wiley + Sons\ Ltd[ KEY WORDS*Community Screening for Dementia "CSI {D|#^screening test^dementia^informant interview^cognitive test^cross!cultural studies Cross!cultural studies of dementia\ particularly those involving developing countries\ o}er a unique opportunity for identifying risk factors by providing a much wider diversity of environ! mental exposures than do studies in industrialized countries where important risk factors may be missed because of their very pervasiveness "Osun! tokun et al[\ 0881^Hendrie\ 0888#[ Cross!cultural studies present the researcher with major methodological problems\ however[ Not least of these problems is developing instru! ments for screening and clinical assessment that minimize cultural biases[ This process is par! ticularly challenging in studies of dementing dis!

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A state of T-cell activation, reflected by a marked degree of spontaneous proliferation in vitro, exists among patients with human T-cell lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) but not in those with retroviral-induced adult T-cell leukemia (ATL). We wished to define the mechanism by which the immune activation of circulating cells from HAM/ TSP is driven, thus gaining insight into the pathogenesis of this HTLV-I-associated disease. By using a modification of the polymerase chain reaction, we compared the levels ofinterleukin 2 (IL-2) and IL-2 receptor a chain (IL-2Ra) mRNA expression to the transcription of the HTLV-I transactivator gene, pX, in peripheral blood mononuclear cells of HAM/TSP and ATL patients as well as seropositive carriers. Up-regulation of IL-2 and IL-2Ra transcripts was detected in HAM/TSP and seropositive carriers that paralleled the coordinate mRNA expression of the pX transactivator. In addition, IL-2 and soluble IL-2Ra serum levels in HAM/TSP and seropositive carriers were elevated. Despite markedly elevated levels of soluble IL2Ra in ATL, transcripts for IL-2 and pX were not demonstrable in the circulating cells. Finally, the marked degree of in vitro spontaneous proliferation present in HAM/TSP was profoundly inhibited by specific anti-IL-2R or anti-IL-2 blocking antibodies.Collectively, these results suggest that immune activation in HAM/TSP, in contrast to ATL, is virally driven by the transactivation and coordinate expression of IL-2 and IL-2Ra. This deregulated autocrine process may contribute to the evolution of inflammatory nervous system damage in HAM/TSP.

HTLV-I is sexually transmitted more efficiently from men to women than vice versa, and the majority of HTLV-I endemic areas report a female preponderance of HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) cases. The objective of this study was to estimate the gender- and age-specific incidence rates of HAM/TSP in the general population as well as in the HTLV-I-infected population in Jamaica and in Trinidad and Tobago. Incidence rates for HAM/TSP were computed based on all reported incident cases in both countries between 1990 and 1994. Population census reports for 1990 were used to calculate the population at risk. The age-standardized HAM/TSP incidence rate (mean +/- standard error of the mean) in Jamaica was 1.8 +/- 0.2/100,000 person years (PY). Among individuals of African descent in Trinidad and Tobago, the rate was 1.7 +/- 0.4/100,000 PY. As in HTLV-I seroprevalence, the incidence rate of HAM/TSP increased with age through the fifth decade of life and was three times as high in women than in men. The HAM/TSP incidence rate, calculated as a function of the number of HTLV-I-infected persons in each age stratum, is higher in women (24.7/100,000 PY) than in men (17.3/100,000 PY). With HTLV-I infection, the lifetime risk of developing HAM/TSP was estimated to be 1.9% overall and is slightly higher in women (1.8%) than in men (1.3%). Thus, the higher prevalence of HTLV-I in women in endemic areas does not fully explain the preponderance of female HAM/TSP, suggesting that other cofactors must be present. The higher incidence rate in women between the ages of 40 and 59 years, as well as the increase in HAM/TSP incidence rates with age, are indicative of the importance of adult-acquired HTLV-I infection, presumably through sexual transmission.

The pathogenesis of human T-cell lymphotropic virus type I (HTLV-I) in adult T-cell leukemia/lymphoma (ATL) and HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP) is poorly understood. We prospectively followed up and evaluated the virologic correlates of infection in transfusion recipients after seroconversion, in asymptomatic carriers, and in ATL and HAM/TSP patients. Proviral DNA levels (copies/105 lymphocytes) were determined by real-time automated polymerase chain reaction and antibody titers by end-point dilution by use of an HTLV-I enzyme-linked immunoassay. In early infection, proviral load was initially elevated (median, 212 copies/105 lymphocytes at time 1) and later decreased (median, 99 copies at time 2, and 27 copies at time 3). Corresponding antibody titers were low at time 1 (1:2154), had significantly increased by time 2 (1:12312), and were stable by time 3 (1:4694). These viral markers were significantly lower in asymptomatic carriers than in HAM/TSP or ATL patients. Therefore, proviral load and antibody titers may be useful as predictive markers of disease among carriers.