Body sway was studied at various body inclinations, voluntarily maintained for about 1 min, in young and elderly normals and in idiopathic parkinsonians. They stood on a dynamometric platform, whose output gave the instantaneous centre of foot pressure (CFP), its mean value and body sway area, with eyes open (EO) or closed (EC). Subjects held the normal upright stance, or the maximum possible inclined posture (body straight, rotated at the ankle joints) in forward or backward direction, or intermediate postures. EMG was recorded from tibialis anterior (TA), soleus (Sol), extensor digitorum brevis (EDB) and flexor digitorum brevis (FDB). The cross-correlation function between the profile of the EMG envelope and the profile of the shift of CFP along the sagittal plane was calculated. In young subjects standing with EO, the maximum extent of antero-posterior (A-P) displacement of CFP was about 60% of foot length. EC reduced this value to about 50%. In the elderly normals, the maximum A-P displacement was about 40% (EO) and 30% (EC). In both groups, sway area was minimal during normal stance with EO and increased progressively when the subjects leant forward or backward. With EC, sway area further increased during normal stance and the rate of increase in relation to inclination augmented markedly. Sol was tonically active during normal stance. Forward leaning increased Sol EMG and induced activity in FDB. TA and EDB were active during backward leaning. The peak of the cross-correlation function between Sol EMG and instantaneous CFP was higher during normal stance than forward inclination, while the reverse was true for FDB. This suggests a role of FDB in the fine-tuning of postural adjustment during forward leaning, and a weight-supporting role of Sol. During backward inclination, TA but not EDB was cross-correlated with CFP. In the parkinsonians, maximum A-P displacement of CFP was just about 30% of foot length (EO; about 20% with EC); its extent was inversely correlated with the severity of the disease. The relationship between sway area and A-P displacement was similar to the elderly, both with EO and EC, within the common range of inclination. In the patients affected by the long-term syndrome, A-P displacement was further reduced while sway area increase at the critical postures was often absent. In all patients, the relationship between muscle activity and body inclination was comparable to normal.(ABSTRACT TRUNCATED AT 400 WORDS)

Epileptic-like activities are observed in mammals exposed to ambient pressures higher than 20 atm. These symptoms are part of the so called "high pressure nervous syndrome". In the search of the cellular mechanisms of this syndrome, we examined synaptic and intrinsic pressure-induced changes in the in vitro hippocampal slice preparation in the rat. We found that pressure (80 atm) depresses the efficiency of excitatory amino acidergic and inhibitory GABA synaptic transmissions, while it increases the intrinsic excitability of the CA1 pyramidal cells and induced multiple population spikes. The changes were associated with a selective increase in the effects of NMDA andL-homocysteate, while the postsynaptic effects of GABA was unchanged. NMDA antagonists and GABA synergistic drugs antagonized the pressure-induced hyperexcitability and multiple population spikes. These results suggest that pressure would decrease transmitter release at the tested excitatory and inhibitory synapses and would facilitate NMDA postsynaptic mechanisms. Thus, changes in both NMDA and GABA processes might be involved in the development of the high pressure nervous syndrome.

The first part of the paper exposes the basic characteristics of the human spasticity which should be modeled: No hypertonia at rest; velocity-dependent myotatic responses, and fatigability. To model a syndrome including these signs is a related but different problem. Results and limits of the clinical neurophysiology concerning the spasticity are briefly quoted. Animal models would better assist the human neurophysiology when having their neuroanatomy closer to the human one. The second part confirms that a local unilateral excision of the ad hoc sensorimotor cerebral cortice of the Baboon induces a permanent palsy of the contralateral foot and leg, and after delay signs of spasticity in the Sol. Neither clasp-knife phenomenon nor fatigability is observed. There is no sign of motoneuron hyper-excitability. A GABA-related pharmacology suggests a significant defect in the presynaptic inhibition of the reflexogenic IA in-put, and possibly a defect in a post-synaptique gabaergic inhibition. Finally the monkey is considered as a valuable support for modeling the human spasticity, symptom and possibly syndrome.

In a previous study we found that the intrinsic excitability of the hippocampal CA1 pyramidal cells increased under helium pressure (80 bar). We presently show that drugs inhibiting gamma-aminobutyric acid (GABA) uptake or facilitating GABA binding partially reversed the pressure-induced hyperexcitability of the CA1 pyramidal cells. When these drugs were simultaneously applied with 2-D,L-aminophosphonovaleric acid, a specific antagonist of N-methyl-D-aspartate (NMDA) receptors, the effect of pressure on the neuronal excitability was nearly abolished. These results suggested that the observed pressure-induced hyperexcitability of pyramidal cells resulted from reduced efficiency of GABA transmission and facilitated excitation mediated by NMDA receptors.

The effect of high helium pressure on inhibitory synaptic transmission was studied in rat hippocampal slices with extracellular recordings. Both feed-forward and recurrent GABAergic inhibition were tested in the CA1 region with paired-pulse stimulation paradigms. The efficiency of both types of inhibition decreased under high pressure (80 atm). However, the depression of synaptic and antidromic field potentials induced by perfusion of GABA or muscimol were not significantly affected by pressure. High pressure induced hyperexcitability of CA1 pyramidal cells. This effect was reduced by the application of 2-aminophosphonovalerate or GABA. The present results suggest that: (1) high pressure reduces the efficiency of the GABAergic inhibitory transmission but does not affect the sensitivity of GABAA receptors; (2) two different processes (reduction of GABAergic inhibition and facilitation of N-methyl-D-aspartate-mediated excitation) might be a direct consequence of the change in the voltage-sensitive ion channels under high pressure and might be involved in the development of the pressure-induced hyperexcitability of CA1 pyramidal cells.

In a previous study, it was shown that helium pressure depressed excitatory synaptic transmission mediated by the Schaffer-commissural afferents and increased the intrinsic excitability of pyramidal cells, in the CA1 region of hippocampal slices in the rat. In the present study, the neurochemical bases of these changes was investigated. Various excitatory amino acids were studied under normal and up to 80 atm of helium. At normal pressure, the amino acids tested induced a decrease in the field excitatory postsynaptic potential (EPSP) and antidromic field potential of CA1 pyramidal cells. These changes probably resulted from the well known depolarizing effect of the compounds.

High pressures of helium affect the physiology of the central nervous system in animals and humans. We examined these effects in rat hippocampal slices. The in vitro preparation displayed a reversible reduction in postsynaptic and antidromic field potentials of CA1 pyramidal cells, but no significant change in the amplitude of the afferent volley. Although the subliminal synaptic response of CA1 neurons was depressed, the ability of these cells to produce population spikes was enhanced. These changes resembled those previously found in vivo in the rat hippocampus. The present results support the hypothesis of a helium pressure-induced depolarization of hippocampal neurons. Other possible mechanisms are discussed.

We examined the influence of helium pressure on the depression induced by various excitatory amino acids in CA1 hippocampal field potentials. The effects of quisqualate, l-glutamate, l-aspartate and kainate were not significantly affected by helium pressure, while those of N-methyl-d-aspartate and d,l-homocysteate were enhanced. These findings suggest that helium pressure specifically increased the sensitivity of the N-methyl-d-aspartate receptor type in the hippocampus. Other hypotheses are discussed.

High pressures affect the physiology of the central nervous system. For a better understanding of this effect, we examined the hippocampal activity in the rat under high pressures (91 bars) of helium-oxygen.

High pressures elicit a high-frequency tremor (8–12 c/sec) in mammals, the mechanisms of which are still unknown. The present study shows that: (1) in spite of many similarities observed between the EMG characteristics of harmaline-induced tremor and pressure-induced tremor, cerebellar lesions which suppress the harmaline-induced tremor, do not modify the characteristics of the pressure-induced tremor; (2) at depth, the caudal part of the spinal cat (section at T9–T10 spinal level) displays irregular spontaneous EMG activities which can be clonic or rhythmic (4–8 c/sec), and a neuromuscular stretch hyperreflexivity. These data suggest that the origin of the pressure-induced tremor is spinal and neuromuscular rather than cerebellar.