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We used two simple tasks to test the capacities of patients with Parkinson's disease to discriminate and identify olfactory stimuli. The patients presented defective odor identification abilities whereas their capacity to discriminate between odors was apparently unaffected. This raises a question about the nature of olfactory dysfunction in Parkinson's disease. Further clinical data is required for analysis of this dysfunction. We therefore propose simple and rapid tests appropriate for clinical use with Parkinson's disease patients.

The chronic effect of L-Dopa administration on the movement-related cortical potentials (MRCPs) was studied in two groups of patients with Parkinson's disease (PD): patients de novo (DN) and patients with on-off fluctuations. The BP and NS' premovement components of MRCPs associated with wrist flexion were assessed by their gradients and by their distribution on the midline (CZ) and the ipsilateral and contralateral hand sensorimotor areas. The treatment efficacy was controlled by a decrease in PD score (Columbia University Rating Scale). The BP component was absent in four out of nine patients DN. After 3 months of treatment, BP and NS' were recorded in six out of seven patients, and the NS' slope was significantly increased in all patients. In the off phase, MRCPs from patients with on-off fluctuations did not present a BP component. In the on phase, the NS' slope was increased and the BP was recorded in two out of nine patients. These patients exhibited an earlier PD stage (Hoehn and Yahr, stage 3). These two patterns of changes in the MRCPs induced by L-Dopa treatment suggest that the BP component was recorded in patients DN when a partial resolution of the nigrostriatal activity could occur. In patients with severe fluctuations, the dopaminergic striatal pathway was more severely affected and the increase of the NS' component demonstrated the activation of extrastriatal dopamine sites within the central nervous system (limbic and cortical structures, in particular).

Cortical potentials associated with voluntary, self-paced wrist flexion (MRPs) were recorded from 3 scalp locations (Cz and psi contralateral hand motor area) in patients with Parkinson's disease (9 de novo patients and 30 L-Dopa treated patients). The analysis concerned 3 components of the MRPs: the 2 slow negative shifts (NS1 and N1) before the movement onset and the motor potential (MP). The NSI amplitude was measured at Cz, the peak negativity N1 and MP from contralateral hand motor area location. The potential distribution was also studied. The amplitude of the MRPs components was the same as in the normals. But in de novo patients, the potential distribution of the NS1 component was different; a Cz preponderance of the NS1 amplitude was not found. In patients treated with L-Dopa, there is a negative correlation between the changes in amplitude and the changes in clinical rating for NS1, N1 and MP components. The decrease in the MRPs components was significant from stage III and IV of the Hoehn and Yahr scales. After L-Dopa therapy, the NS1 component from de novo patients was increased in amplitude. The amplitude of the MRPs components from patients with L-Dopa induced clinical fluctuations was reduced during "off" period in comparison to "on" period. The findings suggest that the NS1 potential and the N1 and MP components share 2 distinct systems for the control of voluntary movement. Their mechanism in Parkinson's disease is discussed.

A reciprocal continuous inhibition by flexor on extensor muscles was proved during Parkinsonian rigidity. Extensor motoneurone excitability was tested by Hoffmann's reflex and flexor activity was altered by lidocaine anaesthesia of the peroneal nerve (PN). During PN anaesthetic block, a gradual increase of Hoffmann's reflex was noted. It was statistically significant at the 15th minute after lidocaine injection, and was maximum at the 30th minute. The reciprocal inhibition was considerable in 16 patients with Parkinsonism, as recorded before treatment. In normal subjects, it was small and non-significant. After one month's treatment with L-dopa at the usual therapeutic dose, this reciprocal inhibition greatly decreased in the same patients. The origin of this reciprocal continuous inhibition is discussed.

Electrophysiological and pharmacological analysis of L-Dopa-induced dyskinesia and tardive dyskinesia (L.DD) due to neuroleptics was performed on 12 patients with Parkinson's disease and on 12 others with psychotic diseases. This analysis included the examination of spinal reflexes, monosynaptic H reflex, polysynaptic cutaneous reflex of the lower limb, muscular responses to passive movement [stretch reflex and shortening reaction (SR)] and the study of the motor response to a dopaminergic stimulus (I.V. injection of Piribedil (PBD), a dopamine agonist). There was no difference in EMG activity between L.DD and TD. Three EMG patterns can be distinguished: anarchic discharge pattern (ADA), tonic grouping discharge pattern (AST) and rhythmic burst pattern (ABR). PBD effects indicate a possible relationship between the EMG patterns and the sensitivity level of the motor dopamine receptors. During L-Dopa dyskinesia and tardive dyskinesia, the same changes in spinal reflexes were observed. Muscle tone tested by muscular responses to passive movement (shortening and myotatic reaction) was normal. Monosynaptic excitability explored by H/M ratio was within the normal range. In contrast, the polysynaptic nociceptive reflex was increased in every case. In Parkinsonian patients with L-Dopa dyskinesia, this pattern of the spinal reflexes was significantly different in comparison to the rigid phase. Intravenous infusion of PBD suppressed tremor and provoked the occurrence of dyskinetic activity in Parkinsonian patients with L-Dopa dyskinesia during the rigid phase. During the dyskinetic phase, as in tardive dyskinesia, PBD increases these phenomena and changes EMG activity in rhythmic pattern. It is suggested that L-Dopa dyskinesia and tardive dyskinesia can be determined by testing EMG activity, spinal reflexes and dopaminergic reactivity. There is evidence to suggest that the various types of involuntary abnormal movement represent a single entity, and that dopamine receptor supersensitivity may be involved.

The effects of a muscle twitch on the tremor of the extensor indicis muscle and of the tibial anterior muscle have been recorded in 14 patients with essential tremor and in 10 patients with Parkinson's disease. The muscle twitch evoked by the electrical stimulation of the motor nerve inhibits the tremor and synchronises it. The mean duration of the inhibition is 92.1 +/- 6.8 ms for essential tremor and 183.0 +/- 16.8 ms for Parkinsonian tremor. This inhibitory phase lasts longer when the muscle twitch is induced during the second half of the Parkinsonian tremor cycle. The effects of voluntary contraction and of unloading suggest that inhibition and resetting of the tremor can be attributed to the autogenic mechanism induced by Ib fibres discharges. The presence of a rhythmic inhibition in the cycle of Parkinsonian tremor accounts for the longer duration of the inhibitory phase. In practice, these techniques aid the diagnosis of tremor in these two conditions, for example they assist the identification of low frequency essential tremor and of postural tremor in Parkinson's disease.

To determine the extent to which deficits in coordination between posture and movement are influenced by postural disorders, postural adjustments associated with rapid voluntary arm movement were studied in PD patients and controls. EMG activity in postural muscles of the lower limbs and the trunk and local anteroposterior accelerations of the upper part of the leg were recorded in subjects who rapidly raised their arms to a horizontal position in response to a visual signal. The arm movement was characterized electromyographically by EMG activity from the deltoid muscle (anterior portion) and kinetically by acceleration of the arm. Study of characteristics of voluntary movement showed a nonsignificant increase in RT (simple-reaction time task) and an important increase in MT. There were important differences between PD patients and control subjects with regard to postural adjustments. Timing between voluntary movement and postural movement was anticipatory in 5% of PD patients, whereas it was anticipatory in 100% of control subjects. In PD patients, organization of early postural adjustments was not specific to voluntary movement; in control subjects, organization of early postural adjustments was specific to the forthcoming movement. Last, a possible functional relation between the "quality" of postural adjustments and a reduction in motor performance of normal subjects is suggested.