It was demonstrated that the soleus H-reflex was depressed for more than 10 s following a preceding passive dorsiflexion of the ankle joint. This depression was caused by activation of large-diameter afferents with receptors located in the leg muscles, as an ischaemic block of large-diameter fibres just below the knee joint abolished the depression, whereas a similar block just proximal to the ankle joint was ineffective. The depression of the H-reflex was not caused by changes in motoneuronal excitability, as motor-evoked potentials by magnetic brain stimulation were not depressed by the same passive dorsiflexion. Therefore it was concluded that the long-lasting depression is due to mechanisms acting at presynaptic level. The transmission of the monosynaptic Ia excitation from the femoral nerve to soleus motoneurones was not depressed by the ankle dorsiflexion. The depression thus seems to be confined to those afferents that were activated by the conditioning dorsiflexion. In parallel experiments on decerebrate cats, more invasive methods have complemented the indirect techniques used in the experiments on human subjects. A similar long-lasting depression of triceps surae monosynaptic reflexes was evoked by a preceding conditioning stimulation of the triceps surae Ia afferents. This depression was accompanied by a reduction of the monosynaptic Ia excitatory postsynaptic potential recorded intracellularly in triceps surae motoneurones, but not by changes in the input resistance or membrane potential in the motoneurones. Stimulation of separate branches within the triceps surae nerve demonstrated that the depression is confined to those afferents that were activated by the conditioning stimulus. This long-lasting depression was not accompanied by a dorsal root potential. It is concluded that the long-lasting depression is probably caused by a presynaptic effect, but different from the "classical" GABAergic presynaptic inhibition which is widely distributed among afferent fibres and accompanied by dorsal root potentials. It is more probably related to the phenomenon of a reduced transmitter release from previously activated fibres, i.e. a homosynaptic post-activation depression. The consequences of this post-activation depression for the interpretation of results on spinal mechanisms during voluntary movements in man are discussed.

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Objectives-Comparative gait analyses in neurological diseases interfering with locomotion are of particular interest, as many hypokinetic gait disorders have the same main features. The aim of the present study was (1) to compare the gait disturbance in normal pressure hydrocephalus and Parkinson's disease; (2) to evaluate which variables of the disturbed gait pattern respond to specific treatment in both diseases; and (3) to assess the responsiveness to visual and acoustic cues for gait improvement. Methods-In study 1 gait analysis was carried out on 11 patients with normal pressure hydrocephalus, 10 patients with Parkinson's disease, and 12 age matched healthy control subjects, on a walkway and on a treadmill. In study 2, patients with normal pressure hydrocephalus were reinvestigated after removal of 30 ml CSF, and patients with Parkinson's disease after administration of 150 mg levodopa. In part 3 visual cues were provided as stripes fixed on the walkway and acoustic cues as beats of a metronome. Results-The gait disorder in both diseases shared the feature of a reduced gait velocity, due to a diminished and highly variable stride length. Specific features of the gait disturbance in normal pressure hydrocephalus were a broad based gait pattern with outward rotated feet and a diminished height of the steps. After treatment in both diseases, the speed increased, due to an enlarged stride length, now presenting a lower variability. All other gait variables remained unaVected. External cues only mildly improved gait in normal pressure hydrocephalus, whereas they were highly eVective in raising the stride length and cadence in Parkinson's disease. Conclusion-The gait pattern in normal pressure hydrocephalus is clearly distinguishable from the gait of Parkinson's disease. As well as the basal ganglia output connections, other pathways and structures most likely in the frontal lobes are responsible for the gait pattern and especially the disturbed dynamic equilibrium in normal pressure hydrocephalus. Hypokinesia and its responsiveness to external cues in both diseases are assumed to be an expression of a disturbed motor planning. (J Neurol Neurosurg Psychiatry 2001;70:289-297)

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