Factor analysis of the Cohen-Mansfield Agitation Inventory in three large samples of nursing home patients with dementia and behavioral disturbance.

OBJECTIVE: Limited work has addressed the construct validity of the Cohen-Mansfield Agitation Inventory (CMAI) in nursing home patients. The authors tested the CMAI factor structure by use of data from three samples of nursing home patients categorized a priori as having at least mild behavioral and psychological symptoms of dementia. METHODS: CMAI data were from the baseline assessment of three randomized, placebo-controlled trials of risperidone for treating elderly nursing home patients. Exploratory factor analyses were conducted on two trials (N = 304; N = 344), and the results of these exploratory factor analyses were then tested with confirmatory factor analysis by use of data from a third trial (N = 617). RESULTS: Principal-components analysis suggested the presence of four factors: 1) Aggressive Behavior (hitting, kicking, scratching, biting, pushing, grabbing, throwing things, cursing or verbal aggression, spitting, tearing things/destroying property, hurting self or others, screaming); 2) Physically Non-Aggressive Behavior (pacing, trying to get to a different place, general restlessness, inappropriate dressing or disrobing, handling things inappropriately, performing repetitious mannerisms); 3) Verbally Agitated Behavior (complaining, constant requests for attention, repetitive questions, negativism); and 4) Hiding and Hoarding. Confirmatory factor analysis indicated that the four-factor solution was a reasonable fit to the data. CONCLUSION: Four factors emerged on the CMAI in nursing home patients with behavioral and psychological symptoms of dementia. The results obtained converge reasonably with previous publications concerning the factor structure of the CMAI, which, taken together, suggest a fairly robust factor structure for the instrument.     

Fucose and fucosyllactose enhance in-vitro hippocampal long-term potentiation

Bath application of -fucose and -fucosyllactose ( F1 increases the potentiation of the population spike amplitude (POP-spike) and the field excitatory postsynaptic potential (fEPSP) after tetanization of the Schaffer collaterals of the rat hippocampus. The ineffective isomers -fucose and 3-fucosyllactose (3-F1) have no such effect. Since not only the maintenance of long-term potentiation LTP is influenced but also its induction is drastically improved, an effect of the sugars via the formation of glycoproteins but also via different actions on induction mechanisms is discussed.     

Concentric sclerosis (Baló): Morphometric and in situ hybridization study of lesions in six patients

Brain tissues from 6 patients with concentric sclerosis (Baló) were examined by in situ hybridization, immunocytochemistry, morphometry, and histological methods. The patients were 24 to 48 years old and had progressive cerebral symptoms and signs that lasted 15 to 100 days. Large demyelinative lesions, most frequent in the frontal white matter, contained alternating bands of demyelinated and partly myelinated white matter that were arranged in concentric or mosaic patterns. In the areas of demyelination, axons were relatively well preserved and there were perivascular inflammatory infiltrates. In 2 specimens, lesions contained regions with the characteristic appearance of actively demyelinating multiple sclerosis plaques. Oligodendroglial densities were highest in normal-appearing white matter, lower in partially myelinated areas, and lowest in demyelinated areas, which also contained many hypertrophic astrocytes closely associated with oligodendroglia. Messenger RNA levels for myelin-related proteins followed the same pattern; they were lowest in demyelinated areas, higher in partially myelinated areas, and highest in normal-appearing white matter beyond lesion margins. Our findings suggest that concentric sclerosis is a variant of multiple sclerosis, that oligodendroglial loss is important in the pathogenesis of demyelination, and that partially myelinated areas probably represent stages of ongoing myelin breakdown rather than remyelination of previously demyelinated areas.