Residual bone-mineral density and muscle strength after fractures of the tibia or femur in children.

This study compared the bone-mineral density in the proximal part of the femur and the flexion and extension strength of the knee in the fractured and the non-fractured limbs after an uncomplicated fracture of the tibia or femur in children. Thirty-eight children, whose ages ranged from two to fifteen years at the time of the injury, were evaluated at an average of 2.3 years after the injury. The mean difference in bone-mineral density between the fractured and non-fractured limbs was 3.3 per cent (p = 0.004). There was no significant difference between the bone-mineral density of the limbs that had been immobilized for less than four weeks and that of the contralateral, non-fractured limbs. However, the mean difference between the bone-mineral density of the limbs that had been immobilized for more than eight weeks and that of the contralateral limbs was 4.3 per cent (p = 0.006). There was little or no relationship between the time since the injury and the difference in bone-mineral density between the two limbs of the patient at the intervals of follow-up that were studied. No residual weakness in flexion and extension of the knee was detected, and no relationship was established between the limb-to-limb differences in strength and the limb-to-limb differences in bone-mineral density. The residual bone-mineral deficit was found to be minimum after an uncomplicated fracture. This difference, while statistically significant, is unlikely to be clinically important in the long term. However, the fact that there was a deficit raises a potential concern for children who have more severe or repeated injuries.     

Sprouting of cholinergic axons does not occur in the cerebral cortex after nucleus basalis lesions.

Different doses of the excitotoxin quisqualate were used to make lesions in the caudal part of the ferret nucleus basalis, i.e. the part that projects to the visual cortex. The higher doses of the excitotoxin destroyed all nerve growth factor receptor-immunoreactive cells in the caudal nucleus basalis and gave rise to up to 75% loss of acetylcholinesterase-containing axons in the visual cortex. In sections stained for Nissl substance there was generalized tissue damage around the injection sites and extensive loss of all neuron types in areas surrounding the caudal nucleus basalis. Lower doses of the excitotoxin damaged only a proportion of the nerve growth factor receptor-immunoreactive neurons in the caudal nucleus basalis and produced a much lower depletion of acetylcholinesterase-positive fibres in the visual cortex. The only damage seen in sections stained for Nissl substance was a loss of magnocellular neurons in the vicinity of the injection sites. A quantitative morphological approach was used to show that either one week or three months after the lesions there was a linear correlation between the proportion of acetylcholinesterase-positive axons lost in the visual cortex and the proportion of nerve growth factor receptor-immunoreactive cells that had disappeared from the caudal nucleus basalis. Since the correlation lines for the short-term (one week) survival and the long-term (three months) survival experiments coincided, this indicated that no collateral sprouting of cholinergic axons had occurred in the visual cortex of the long-term survival animals regardless of size of the lesion in the nucleus basalis.