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1.  Delusions and Hallucinations Are Associated With Worse Outcome in Alzheimer Disease 
Archives of neurology  2005;62(10):1601-1608.
Delusions and hallucinations are common in Alzheimer disease (AD) and there are conflicting reports regarding their ability to predict cognitive decline, functional decline, and institutionalization. According to all previous literature, they are not associated with mortality.
To examine whether the presence of delusions or hallucinations has predictive value for important outcomes in AD.
Design, Setting, and Participants
A total of 456 patients with AD at early stages (mean Folstein Mini-Mental State Examination [MMSE] score of 21 of 30 at entry) were recruited and followed up semiannually for up to 14 years (mean, 4.5 years) in 5 university-based AD centers in the United States and Europe. Using the Columbia University Scale for Psychopathology in AD (administered every 6 months, for a total of 3266 visit-assessments, average of 7.2 per patient), the presence of delusions and hallucinations was extracted and examined as time-dependent predictors in Cox models. The models controlled for cohort effect, recruitment center, informant status, sex, age, education, a comorbidity index, baseline cognitive and baseline functional performance, behavioral symptoms, and use of neuroleptics and cholinesterase inhibitors.
Main Outcome Measures
Cognitive (Columbia MMSE score of ≤20/57 [approximate Folstein MMSE score of ≤10/30]), functional (Blessed Dementia Rating Scale [parts I and II] score of ≥10), institutionalization equivalent index, and death.
During the full course of follow-up, 38% of patients reached the cognitive, 41% the functional, 54% the institutionalization, and 49% the mortality end point. Delusions were noted for 34% of patients at baseline and 70% at any evaluation. Their presence was associated with increased risk for cognitive (risk ratio [RR], 1.50; 95% confidence interval [CI], 1.07-2.08) and functional decline (RR, 1.41; 95% CI, 1.02-1.94). Hallucinations were present in 7% of patients at initial visit and in 33% at any visit. Their presence was associated with increased risk for cognitive decline (RR, 1.62; 95% CI, 1.06-2.47), functional decline (RR, 2.25; 95% CI, 1.54-2.27), institutionalization (RR, 1.60; 95% CI, 1.13-2.28), and death (RR, 1.49; 95% CI, 1.03-2.14).
Delusions and hallucinations are very common in AD and predict cognitive and functional decline. Presence of hallucinations is also associated with institutionalization and mortality.
PMCID: PMC3028538  PMID: 16216946
2.  Gray matter MRI T2 hypointensity predicts longitudinal brain atrophy in multiple sclerosis 
Archives of neurology  2005;62(9):1371-1376.
Gray matter MRI T2-hypointensity, a marker of iron deposition, is associated with clinical impairment and brain atrophy in cross-sectional studies of multiple sclerosis (MS). Treatment with intramuscular interferon beta-1a limits brain atrophy in the second year of treatment.
We tested whether T2-hypointensity predicts brain atrophy and whether interferon impacts on this relationship.
We performed a post-hoc analysis of patients with MS from a two year clinical trial of interferon beta-1a (30ug IM weekly) or placebo. We determined deep gray matter T2-hypointensity, brain parenchymal fraction (BPF), and total T2-, gadolinium-enhancing-, and T1-lesion volumes.
T2-hypointensity in various gray matter areas correlated with baseline BPF (r=.19 – .39, p=.001 –.029). In placebo-treated patients (n=65), baseline T2-hypointensity predicted the change in BPF in the first year and over two years (r=.26 – .42; p <.001 – .032). T2 hypointensity was chosen in regression modeling as the best predictor of BPF change at the one year (R2=.23, p=.002) and two year (R2=.33, p<.001) time points after accounting for all MRI variables. In the interferon group (n=68), there was no relationship between baseline T2-hypointensity and BPF change.
Gray matter T2-hypointensity predicts the progression of brain atrophy in placebo but not interferon-treated patients. This predictive effect is seen as early as in the first year. We hypothesize that interferon-beta may exert its effect on brain atrophy in part by reducing a cascade of events involving iron deposition as a mediator of neurotoxicity or as a disease epiphenomenon.
PMCID: PMC1435740  PMID: 16157744

Results 1-2 (2)