The relationship between neuropsychological function and brain damage detected by neuroimaging after closed head injury

Studies relating neuropsychology and structural neuroimaging after closed head injury are reviewed. Particular attention is given to the question of the relative contribution of focal and diffuse damage to neuropsychological impairment. The evidence currently available emphasizes the importance of diffuse damage in closed head injury. Diffuse damage is not equally distributed in the brain, and the review suggests three axes that are relevant for neuropsychological function: (1) damage may be unilateral or bilateral, (2) damage is characteristically greater in anterior regions than posterior regions, and (3) damage shows a centripetal gradient. A large gap remains between the emergent generalizations concerning head injury and reliable neuropsychological interpretation of scans from individual patients.     

Bone mass and body composition in normal women.

The interrelationships between measurements of bone mass and total-body bone mineral were examined in a cross-sectional study of normal healthy women aged 17-82 years. In addition we evaluated the relationship between measures of body composition, estimated by four independent techniques, and bone mass in the same population. Considering the group as a whole, bone mass at all sites correlated with each other and with total-body bone mineral (TBBM). Cancellous and cortical sites could predict TBBM equally well. As expected, all measurements of bone mass were significantly lower in postmenopausal women in comparison to premenopausal women. Declines in bone mass were only seen in premenopausal women in the femoral neck and Ward's triangle, not in lumbar spine, radius, or skeleton as a whole. In postmenopausal women bone mass correlated negatively with age and years from menopause equally at all sites. TBBM was significantly related to height and weight in both premenopausal and postmenopausal women. In premenopausal and postmenopausal women TBBM also correlated with fat mass, but TBBM was much better correlated with percentage body fat in premenopausal than postmenopausal women. TBBM was a constant proportion of lean body mass in premenopausal women, but the fraction of lean mass occupied by the skeleton declined with age in postmenopausal women. Correction of TBBM for lean mass did not change the relationship between TBBM and percentage fat in premenopausal women but eliminated the relationship in postmenopausal women. Regional measurements, which are at least partially corrected for body size by dividing mass by area, correlated less well with height and weight and with any index of obesity, especially in postmenopausal women.     

A continuous striatal infusion of 6-hydroxydopamine produces a terminal axotomy and delayed behavioral effects

Rat models of Parkinson's disease typically employ a rapid nigral injection of 6-hydroxydopamine (6-OHDA) to produce a near-complete loss of nigrostriatal dopamine neurons, and thus model end stage disease. The present report describes the use of a continuous, low dose infusion of 6-OHDA into the striatum which produces a terminal axotomy of nigrostriatal dopamine neurons and protracted behavioral response. A solution of 6-OHDA in 0.4% ascorbate, delivered at 37°C from osmotic minipumps, was stable for 8 days as determined by its retained toxicity to a dopaminergic neuroblastoma cell line. The continuous infusion of 0.2 μg 6-OHDA per h did not affect the striatal uptake of [³H]GABA, [³H]choline, or [³H]glutamate but reduced [³H]dopamine uptake by 55% within 1.5 days after the start of the infusion. The striatal infusion of 6-OHDA produced a dose-dependent reduction of striatal dopamine and DOPAC levels but did not alter HVA, 5-HT, or 5-HIAA. An increase in amphetamine-induced ipsiversive rotations occurred within 1.5 days after the acute striatal injection of 20 μg or 30 μg of 6-OHDA but required 4 days to develop with the continuous 6-OHDA infusion. The topography of the lesion mapped by [³H]mazindol binding showed that, begining by 1.5 days, a diffuse depletion of terminals encompassed much of the striatum in the 30 μg acute injection group, whereas in the continuously infused rats, the lesion was apparent only by 4 days and was restricted to a smaller and more completely lesioned area. Unlike acutely lesioned animals, continuously infused rats revealed no obvious loss of dopamine neurons in the pars compacta by 5 weeks after 6-OHDA. The continuous striatal infusion of 6-OHDA can produce a topographically limited terminal axotomy of dopamine neurons and a protracted behavioral impairment.