SUMMARY1. In recordings from the human supraorbital nerve with tungsten microelectrodes, eleven afferent units with unmyelinated (C) axons were identified on the basis of their conduction velocities (0-6-1-4 m/s).2. Eight units had low mechanical thresholds (< 0-23 g) and could be activated up to their maximal firing rates of about 100 impulses/s by weak tactile stimuli, whereas three units had higher thresholds (5 5 g) and responded vigorously to noxious stimuli only.3. During a skin indentation the low-threshold units adapted to an irregular lowfrequency discharge, and release of the stimulus elicited a prominent off-response often ending with an after-discharge. Slow stroking was a particularly effective stimulus, even when done with cotton wool, whereas rapid stroking reduced the response. All types of stroking stimuli were occasionally followed by after-discharges. Repeated mechanical stimulation at short intervals resulted in a decline of the response, indicating receptor fatigue. For two units a response to skin cooling was observed.4. The above low-threshold C units have all the main characteristics of the C mechanoreceptors known from the cat and primates but not previously proven to exist in man. The high-threshold C units are similar to the polymodal nociceptors found in other human skin areas.

Ectopically generated and antidromically conducted nerve impulses were recorded in 5 patients with tungsten microelectrodes inserted into skin nerve fascicles. All patients had mainly positive sensory symptoms and reported paresthesiae which could be provoked by different maneuvers which suggested increased mechanosensitivity of the primary sensory neurons at different anatomic levels. Ectopic multiunit nerve activity correlating in intensity and time course to the positive sensory symptoms was recorded: when Tinel's sign was elicited in a patient with entrapment of the ulnar nerve at the elbow, when paresthesiae were provoked by elevation of the arm in a patient with symptoms consistent with a thoracic outlet syndrome, when paresthesiae were evoked by straining during chin-chest maneuver in a patient with an S1 syndrome due to a herniated lumbar disc, when a painful Lasegue's sign occurred during the straight-leg raising test in a patient with an S1 syndrome due to root fibrosis, and when Lhermitte's sign was elicited by neck flexion in a patient with multiple sclerosis. The sites for the ectopic impulse generation in these cases are suggested to be peripheral nerve, brachial plexus, dorsal root or dorsal root ganglion and dorsal columns. The paresthesiae were non-painful except in the patient with Lasegue's sign and the ectopic impulses were probably recorded from large myelinated afferent fibers.

Prompted by previous reports on muscle thixotropy, we have investigated changes in inherent and reflex stiffness of the finger flexor muscles of human subjects at rest, following transient conditioning manoeuvres involving contractions and/or length changes of the finger flexors. The stiffness measurements were combined with electromyographic recordings from forearm and hand muscles and with microneurographic recordings of afferent stretch responses in finger flexor nerve fascicles. Finger flexor stiffness was evaluated by measuring (a) the flexion angle of the metacarpo-phalangeal joints at which the system during rest balanced the force of gravity and (b) the speed and amplitude of angular finger extensions induced by recurrent extension torque pulses of constant strength delivered by a torque motor. In the latter case, extension drifts in the resting position of the fingers were prevented by a weak flexion bias torque holding the fingers in a pre-determined, semiflexed position against a stop-bar. Stiffness changes following passive large amplitude finger flexions and extensions were studied in subjects with nerve blocks or nerve lesions preventing neurally mediated contractions in the forearm and hand muscles. Inherent stiffness was enhanced following transient finger flexions and reduced following transient finger extensions. The after-effects gradually declined during observation periods of several minutes. Similar results were obtained in subjects with intact innervation who succeeded during the pre- and post-conditioning periods in keeping the arm and hand muscles relaxed (i.e. showed no electromyographic activity). In these subjects it was also found that the after-effects were similar for active and passive finger movements and that isometric voluntary finger flexor contractions loosened the system in a way similar to finger extensions. In some subjects electromyographic reflex discharges appeared in the finger flexors in response to the extension test pulses. When elicited by small ramp stretch stimuli of constant amplitude, the stretch reflex responses were found to vary in strength in parallel with the changes in inherent stiffness following the various conditioning manoeuvres. The strength of the multi-unit afferent stretch discharges in the muscle nerve, used as index of muscle spindle stretch sensitivity, varied in parallel with the changes in inherent stiffness. Post-manoeuvre changes in muscle spindle stretch sensitivity were seen also when the spindles were de-efferented by a nerve block proximal to the recording site. The results can be explained in terms of thixotropic behaviour of extra- and intrafusal muscle fibres.(ABSTRACT TRUNCATED AT 400 WORDS)

It is an old observation that non‐volitional arm abduction movements accompanied by a sensation of arm lightness often occur as an after‐effect following forceful voluntary arm abductor contractions against a restraint. In the present study we have tested the hypothesis that such non‐volitional, so‐called ‘postural after‐contractions’ are tonic reflex responses to an enhanced resting discharge in primary muscle spindle afferents which in turn is a consequence of thixotropy‐dependent enhanced stiffness of intrafusal muscle fibres. Results obtained in ten volunteers show that the arm abductor after‐contraction phenomenon in man is most readily evoked by a type of conditioning procedure which in various respects mimics the procedure proven in animal experiments to be particularly effective in producing thixotropy‐dependent excitation of primary spindle endings. It is also shown that changes in arm abductor intramuscular temperature affect the strength of the after‐contractions in a direction predicted by the thixotropy hypothesis. Attention is drawn to several similarities between the after‐contraction phenomenon with accompanying sensory illusions and the tonic reflex responses and illusions that can be induced when primary spindle endings are excited by muscle vibration. The results support our hypothesis that postural after‐contractions are induced by activity in primary muscle spindle afferents as a consequence of thixotropic properties of intrafusal muscle fibres. Central excitability changes following the conditioning voluntary effort may contribute to the phenomenon.

SUMMARY1. A local anaesthetic drug was injected around the peroneal nerve in healthy subjects in order to investigate whether the resulting loss in foot dorsiflexion power in part depended on a y-fibre block preventing 'internal' activation of spindle end-organs and thereby depriving the a-motoneurones of an excitatory spindle inflow during contraction. The motor outcome of maximal dorsiflexion efforts was assessed by measuring firing rates of individual motor units in the anterior tibial (t.a.) muscle, mean voltage e.m.g. from the pretibial muscles, dorsiflexion force and range of voluntary foot dorsiflexion movements. The tests were performed with and without peripheral conditioning stimuli, such as agonist or antagonist muscle vibration or imposed stretch of the contracting muscles.2. As compared to control values of t.a. motor unit firing rates in maximal isometric voluntary contractions, the firing rates were lower and more irregular during maximal dorsiflexion efforts performed during subtotal peroneal nerve blocks. During the development of paresis a gradual reduction of motor unit firing rates was observed before the units ceased responding to the voluntary commands. This change in motor unit behaviour was accompanied by a reduction of the mean voltage e.m.g. activity in the pretibial muscles.3. At a given stage of anaesthesia the e.m.g. responses to maximal voluntary efforts were more affected than the responses evoked by electric nerve stimuli delivered proximal to the block, indicating that impaired impulse transmission in a motor fibres was not the sole cause of the paresis.4. The inability to generate high and regular motor unit firing rates during peroneal nerve blocks was accentuated by vibration applied over the antagonistic calf muscles. By contrast, in eight out of ten experiments agonist stretch or vibration caused an enhancement of motor unit firing during the maximal force tasks.5. The reverse effects of agonist and antagonist vibration on the ability to activate the paretic muscles were evidenced also by alterations induced in mean voltage e.m.g. activity, dorsiflexion force and range of dorsiflexion movements.* To whom correspondence and reprint requests should be sent.

Surprising sensory stimuli causing arousal are known to evoke short‐lasting activation of human sympathetic activity in skin but not in muscle nerves; anecdotal observations suggest that there may even be an inhibition of muscle sympathetic nerve activity (MSNA). To test this hypothesis we recorded multiunit MSNA in the peroneal nerve in 19 subjects aged 19–71 years, while sensory stimuli, consisting of either an electrical skin stimulus to a finger or a visual flash, were delivered repeatedly with intervals of approximately 20 s. The stimuli were given either 200 or 400 ms after the R wave of the electrocardiogram. Dummy stimuli, consisting of trigger pulses without sensory stimulation served as controls. Electrical skin resistance reductions were monitored from the palm of a hand as electrodermal signs of arousal‐induced cutaneous sympathetic activity. On a group basis both types of sensory stimuli attenuated the amplitude of one or two bursts of MSNA, while no such effects occurred after dummy stimuli. Individually, the inhibition was evoked by at least one stimulus modality or delay in 16 subjects whereas in three subjects no significant inhibition occurred. Skin resistance responses were evoked in all subjects. Some subjects responded to one, others to both stimulus modalities, and electrical stimuli were more effective than visual stimuli in causing MSNA inhibition as well as skin resistance reduction. On the other hand, electrodermal signs of arousal were equally common in subjects with and without inhibitory responses. We suggest that the MSNA inhibition evoked by sensory stimuli is an arousal effect which varies markedly between individuals.

1. In fifteen healthy volunteers, muscle nerve sympathetic activity (MSA) was recorded from the peroneal nerve using microneurography. Blood pressure and electrocardiogram were also recorded. 2. Painful stimuli, adjusted to the subject's tolerance level, were delivered over 30‐60 s via (a) pressure to the nail‐bed of different digits, and to the trigeminal region, (b) electrical stimulation (5 Hz) of digital nerves and of the supraorbital nerve, or (c) instillation of soap solution into one eye. Non‐painful ocular pressure was also applied. 3. All procedures except electrical stimulation of digital nerves caused a marked increase in MSA (mean, 160‐248%) with preserved pulse synchrony and a rise in blood pressure. Stimulation of digits induced tachycardia, whereas stimulation of the trigeminal region tended to cause bradycardia. 4. Despite similar pain ratings, electrical stimulation of digital nerves caused a smaller MSA response than the other stimuli (mean increase, 40%). 5. It is concluded that sustained noxious stimulation in awake humans evokes a generalized MSA increase; the activity is still under baroreflex control, but the inhibitory level is reset. Both spinal and brainstem reflexes may contribute; a defence reaction is an unlikely explanation. It is suggested that the number of afferent C fibres activated by electrical stimulation of digital nerves was insufficient to induce any marked MSA response. 6. The non‐painful oculo‐cardiac reflex is associated with a strong increase in MSA.

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