No abstract

The purpose of this study was to compare the amplitude of the flexion reflex of the biceps femoris muscle (BF) with the intensity of the painful sensation elicited by a nociceptive stimulation resulting from application of constant-current either on the sural nerve or on the skin in its distal receptive field. Experiments were carried out on 15 normal volunteers. It was observed that: (1) Stimulation of the sural nerve (either on or through the skin) elicits two different reflex responses in the BF: the first (RII) is of short latency, low threshold and corresponds to a tactile reflex. The second (RIII) is of longer latency and higher threshold, and corresponds to a nociceptive reflex. The threshold of RIII was found to be the threshold of a pain sensation. (2) Stimulation of the skin elicits only a late nociceptive (RIII) response in the BF. The threshold of this response was also found to be that of pain. (3) The threshold of both pain and RIII were found to be higher for sural nerve stimulation (10 mA) than for cutaneous stimulation (5 mA). It was suggested that the large diameter cutaneous fibers could have an inhibitory effect of both pain and the nociceptive reflex. This was supported by the results obtained during a selective ischemic block of the largest diameter fibers in the sural nerve, when a 10 mA stimulation was applied to the nerve. In this case, a decrease of the RII reflex was observed in BF, together with an increase of both RIII and pain sensation. Functional implications of these results are discussed.

The nociceptive flexion reflex (RIII reflex) and the concurrent subjective pain score elicited by right sural nerve stimulation at random intensities were studied in 10 healthy volunteers. A close relationship was found between the recruitment curves of the reflex and the pain score as a function of stimulus intensity. As a consequence, the threshold of the RIII reflex (Tr) and of pain sensation (Tp) were found to be almost identical (mean: 9.8 and 11.3 mA, respectively). Similarly, the threshold for obtaining a maximal reflex response (Tmr) was found to be very close to that for intolerable pain (Tip): 33.5 and 35.1 mA, respectively. These four parameters were studied before and during the immersion of the left hand into a heated thermoregulated waterbath at various temperatures (from 40 to 47.5 degrees C). While nonnociceptive temperatures (40 to 44 degrees C) were without effect, higher conditioning temperatures induced an increase in the four thresholds. In addition, a highly significant linear relationship was observed between the increase in these thresholds and the intensity of the conditioning stimulus in the 44 to 47.5 degrees C range. These four parameters were also studied before and during three other nociceptive conditioning stimuli: immersion of the left hand into a 6 degrees C waterbath, 10 watts muscular exercise of the left hand performed under ischaemia and a painful (5.5 kg/cm2) pinch applied on the nasal septum. These three conditioning situations induced a very significant increase of the four thresholds considered in this study with the greatest being observed during nociceptive cold applied to the left hand. During all the conditioning situations, variations in Tr and Tp as well as in Tmr and Tip were found to be linearly related. This indicates a close relationship between the effects of the conditioning nociceptive stimuli on the reflex and the related pain sensation. These results suggest that the modulation of pain by heterotopic nociceptive stimuli can be explained at least in part by a depression in the transmission of nociceptive messages at the spinal level. They are discussed with reference to the counterirritation phenomena and common features with 'diffuse noxious inhibitory controls' (DNIC) are underlined.

Although normal subjects do not move during REM sleep, patients with Parkinson's disease may experience REM sleep behaviour disorder (RBD). The characteristics of the abnormal REM sleep movements in RBD have, however, not been studied. We interviewed one hundred consecutive non-demented patients with Parkinson's disease and their bed partners using a structured questionnaire assessing the presence of RBD. They rated the quality of movements, voice and facial expression during RBD as being better, equal or worse than in awake ON levodopa condition. Night-time sleep and movements were video-monitored during polysomnography in 51 patients to evaluate the presence of bradykinesia, tremor and hypophonia during REM sleep. Fifty-nine patients had clinical RBD with 53/59 bed partners able to evaluate them. All 53 (100%) reported an improvement of at least one component of motor control during RBD. By history, movements were improved in 87% patients (faster, 87%; stronger, 87%; smoother, 51%), speech was better in 77% patients (more intelligible, 77%; louder, 38%; better articulated, 57%) and facial expression was normalized in 47% patients. Thirty-eight per cent of bed partners reported that movements were 'much better', even in the most disabled patients. The videomonitored purposeful movements in REM sleep were also surprisingly fast, ample, coordinated and symmetrical, without obvious sign of parkinsonism. The movements were, however, jerky, violent and often repetitive. While all patients had asymmetrical parkinsonism when awake, most of the time they used the more disabled arm, hand and leg during the RBD (P = 0.04). Movements involved six times as often the upper limbs and the face as the lower limbs (OR: 5.9, P = 0.004). The percentage of time containing tremor EMG activity decreased with sleep stages from 34.9 6 15.5% during wakefulness, to 3.6 6 5.7% during non-REM sleep stages 1-2, 1.4 6 3.0% during non-REM sleep stages 3-4, and 0.06 6 0.2% during REM sleep (in this last case, it was subclinical tremor). The restored motor control during REM sleep suggests a transient 'levodopa-like' reestablishment of the basal ganglia loop. Alternatively, parkinsonism may disappear by REM sleep-related disjunction between pyramidal and extrapyramidal systems. We suggest the following model: the movements during the RBD would be generated by the motor cortex and would follow the pyramidal tract bypassing the extrapyramidal system. These movements would eventually be transmitted to lower motor neurons because of brainstem lesions interrupting the pontomedullary pathways which mediate the REM sleep atonia.