Search

Signals associated with the command the brain sends to muscles are thought to create the sensation of heaviness when we lift an object. Thus, as a muscle is weakened by fatigue or partial paralysis (neuromuscular blockade), the increase in the motor command needed to lift a weight is thought to explain the increasing subjective heaviness of the lifted object.With different fatiguing contractions we approximately halved the force output of the thumb flexor muscles, which were then used to lift an object. For two deafferented subjects the perceived heaviness of the lifted object approximately doubled, in keeping with the central-signal theory. However, for normal subjects this resulted in objects feeling the same or lighter, inconsistent with the central-signal theory but consistent with the expected effects of the conditioning contractions on the sensitivity of peripheral receptors. In separate experiments we subjected the forearm muscles to complete paralysis with a non-depolarising neuromuscular blocking agent and then allowed them to recover to approximately half-force output. This also resulted in objects feeling lighter when lifted by the semi-paralysed thumb, even though the motor command to the motoneurons must have been greater. This is readily explained by reduced lift-related reafference caused by the prolonged paralysis of muscle spindle intrafusal fibres.We conclude that peripheral signals, including a major contribution from muscle spindles, normally give rise to the sense of exerted force. In concept, however, reafference from peripheral receptors may also be considered a centrally generated signal that traverses efferent and then afferent pathways to feed perceptual centres rather than one confined entirely to the central nervous system. These results therefore challenge the distinction between central- and peripheral-based perception, and the concept that muscle spindles provide only information about limb position and movement.

1. Motor memory and the sense of effort have been investigated in a man with a complete large fibre sensory neuropathy for over 16 years. The perceptions of pain, heat, cold and muscular fatigue remained but he was without perceptions of light touch and proprioception below the neck. 2. The subject was able to discriminate weights held in the hand with an accuracy only slightly worse than control subjects (20 g in 200 g) when forearm movement and visual inspection were allowed. With eyes shut however he could only distinguish a weight of 200 g from 400 g. It is concluded that a crude sense of effort remains which may have a peripheral origin. 3. A limited motor memory was also present, which allowed him to maintain a posture or continue a simple repetitive movement. No novel movement was possible without visual feedback. 4. Differences in movement ability between this subject and others with similar if less pure sensory neuropathies are ascribed to rehabilitation.

A comparison is presented of the latencies of corticofugal effects from the contralateral somatosensory cortex (SI) onto the cat's dorsal column nuclei (d.c.n.) under pentobarbitone anaesthesia. The latencies for transmission in the ascending pathway from d.c.n. to SI after stimulation within the gracile and cuneate nuclei were found to be 3.3 ms for the former and 2.8 ms for the latter. The time courses of inhibition of a medial lemniscal mass response following cortical conditioning and evoked by stimulation of peripheral nerves were measured. All latencies were corrected to exclude the different times taken for stimuli to reach the nuclei from the two limbs. The optimal condition-test interval was 12 ms with a duration of 14.3 ms for the superficial radial nerve (s.r.n.) and 45 ms and 30 ms respectively for the medial plantar nerve (m.p.n.). In each case cortical conditioning inhibited the wave by about 50%. The effect of cortical conditioning upon spontaneously firing d.c.n. single units was investigated. For cuneate cells the mean latency was 6.8 ms and the mean duration 36.8 ms. For gracile cells the latency of onset of inhibition was 17.2 ms and its duration 129 ms. In 75% of cells mixed effects were seen with facilitation preceding inhibition. The latencies of 'corticofugal reflex' action on the gracile and cuneate nuclei after stimulation of the s.r.n. and m.p.n. were determined. The gracile response had a latency approximately 4 times that for the cuneate response. The temporal asymmetry of these corticofugal effects suggests that the pathway is not purely a simple feed-back loop, but may be concerned in other physiological contexts, some of which are discussed.