Control mechanisms for restoring posture and movements in paraplegics.

The control mechanisms underlying undisturbed movements were analysed in two series of experiments: (1) normal physiological responses were investigated in neurologically intact subjects; (2) an artificial motor control system for paraplegic patients using functional neuromuscular stimulation (FNS) of the paralysed leg muscles was developed and tested. In both series of experiments standing-up from a chair and sitting-down were studied. A three-link model of the human body was used for recording and processing biomechanical data. In 5 normal subjects ground reaction forces and the surface electromyogram of different leg muscles were also recorded. Basic physiological aspects of FNS such as muscle force regulation and fatigue could be documented. For the standing-up and sitting-down experiments in 2 paraplegic patients the gluteal and quadriceps muscles were stimulated. The best results were achieved with a combination of open-loop and closed-loop stimulation with position and velocity feedback. The importance of feedforward and feedback control during undisturbed movements is discussed for natural and artificial motor control systems. It is concluded that the control of knee joint angle during standing-up and sitting-down represents an unstable system which cannot be controlled open-loop only. Different aspects of sensory feedback including the regulated variables, gain and stability of the system are discussed on the basis of the experimental data and the literature.

Nonresident macrophages in peripheral nerve of rat: effect of silica on migration, myelin phagocytosis, and apolipoprotein E expression during Wallerian degeneration.

The selective toxicity of silica quartz dust to macrophages was used to assess the role of these cells in Wallerian degeneration and nerve repair. Left sciatic nerves of adult Wistar rats were crushed and one group of animals received repetitive intraperitoneal injections of silica (200 mg two times per week starting 1 day prior to injury), whereas the control group received saline. Unexpectedly, silica treatment did not impair the initial invasion of (hematogenous) macrophages into the degenerating distal nerve stump as revealed by histological and immunocytochemical methods. However, 4 weeks after the lesion three specific events in Wallerian degeneration were significantly inhibited in silica-treated animals: 1) inhibition of phagocytosis and degradation of myelin, 2) delay in disappearance of nonresident macrophages from regenerating nerve, 3) reduction of synthesis and/or secretion of apolipoprotein E in resting macrophages. On the other hand, axonal regrowth and remyelination were not affected by silica. These in situ experiments support and extend previous studies suggesting specific functions for nonresident macrophages in Wallerian degeneration of peripheral nerve.

A correlative study of internode proportions and sensitivity to procaine in regenerated frog sciatic nerves.

A comparison of regenerated and normal frog sciatic nerves showed a marked reduction in conduction velocity from 37.5 to 15.2 m/s with little change in the absolute refractory period. Changes in conduction velocity corresponded to a reduced mean axon caliber (4.8 versus 6.6 micron). Regenerated nerves also had markedly foreshortened internodes (mean of 309 versus 1236) micron) and thinner sheaths than controls. The geometric proportions of internode length/fiber caliber (l/d) was reduced to approximately one-third of normal. Regenerated nerves were more easily blocked by exposure to 3 mmol/liter procaine than controls, showing greater increase in the absolute refractory, or decreases, respectively, in the peak of the alpha-wave and the area of the compound action potential; the effect of procaine on conduction velocity was less marked. Exposure of various lengths of nerves in chambers of 1, 3, or 20 mm length revealed greater differences for the shorter chambers. The data indicated that some effects could be attributed to the foreshortening of the regenerated internodes. The main difference between normal and regenerated nerves, however, had to be attributed to changes in the nodal membrane characteristics of the latter.

Conduction velocity varies with osmotically induced changes of the area of the axon's profile.

The conduction velocity of frog ischiadic nerves incubated in vitro in osmolarities between 220 and 1000 mOsm decreased with the degree of fiber shrinkage. The latter (non-circularity factor) was determined from computer-assisted measurements in freeze-substituted or in chemically fixed fibers. Freeze-substituted normal nerves had a non-circularity factor of 0.91 for fibers of all calibers, which likely reflects the in vivo state of the fiber population. Chemically fixed nerves had a non-circularity factor near 0.68, consistent with previous data. Non-circularity factors decreased with increasing osmolarities of the media, regardless of the type of tissue preparation. Conduction velocity decreased with decreasing non-circularity. Restoration of the nerves to normotonic media increased conduction velocity. The rates of change were accelerated in nerves chemically desheathed with Triton. The decrease in the conduction velocity in osmotically shrunken nerves did not correspond to changes in the absolute refractory period for the propagation of the impulse, used as a sensitive index of non-specific damage. These experimental observations corroborate data from computer simulation of relative sensitivities of nodal and internodal parameters.