PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Proprioception”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,009 records · Page 56Linked to original sources

[Singular clinical form of intramedullary cavity revealed by a loss of proprioceptive sensation in the upper limbs].

A 47-year-old woman developed a progressive sensory deficit of the upper limbs. She lost perception of joint position, vibratory sense, skin-writing and stereognosis. Repeated tests by several examiners, up to 10 years after the onset, demonstrated normal pain and temperature sensation. The right hypoglossal nerve was involved at a late stage of the disease. CT and MRI showed an intramedullary cavity from C1 to T7. Somato-sensory evoked potentials from stimulation of the median nerves confirmed the bilateral impairment of the lemniscal pathways.

Arm↗

Parallel processing of proprioceptive signals by spiking local interneurons and motor neurons in the locust.

The connections made by afferents from a proprioceptor at the femorotibial joint in a hind leg of a locust, the femoral chordotonal organ (FCO), were determined by making intracellular recordings from motor neurons and spiking local interneurons in the central nervous system and from afferent cell bodies in the periphery. Staining the central projections of the afferent neurons with dye introduced into their axons at the receptor, and the intracellular injection of dye into motor neurons and interneurons, shows that the branches of all 3 types of neuron overlap in specific regions of neuropile. Afferents excited by a movement of the receptor apodeme that is equivalent to an imposed extension of the femorotibial joint excite flexor tibiae motor neurons and some spiking local interneurons with cell bodies at the ventral midline of the metathoracic ganglion. The opposite movement excites extensor tibiae motor neurons and a different set of spiking local interneurons. Spikes in afferents that excite flexor motor neurons evoke depolarizing potentials that follow each spike with a consistent central latency of approximately 1.5 msec. The amplitude of the depolarizing potentials is dependent upon the membrane potential of the motor neuron. This evidence points to the connection being direct and to the potentials' being EPSPs. Simultaneous recordings from certain spiking local interneurons and certain flexor motor neurons show that they receive many synaptic potentials in common and are driven in a parallel fashion by movements of the receptor apodeme. Spikes of some afferents evoke EPSPs in both neurons with the same consistency and latency. An afferent can therefore synapse directly upon a motor neuron and a spiking local interneuron. Each afferent synapses on several motor neurons and possibly upon several interneurons. In turn, each motor neuron and each interneuron receives inputs from several afferents.

Animals↗

Afferent perturbations during "monopodal" swimming movements in the turtle: phase-dependent cutaneous modulation and proprioceptive resetting of the locomotor rhythm.

Locomotion consists of a repeating series of movement cycles (locomotor rhythm) with an orderly activation of musculature during each movement cycle (intracycle motor pattern). The effects of sensory stimulation, on both the intracycle motor pattern and the locomotor rhythm, were examined during electrically elicited swimming movements of a single turtle hindlimb. The resulting "monopodal" swimming was not subject to movement-related reflexes from other limbs or postural constraints, and provided a sensitive system for analyzing the effects of transient sensory perturbations. During "monopodal" swimming, cutaneous and extensor muscle-nerve stimulation (single 0.1- to 0.3-msec electrical pulse) had similar phase-dependent effects on the swim cycle in progress. Stimuli delivered during the powerstroke (limb retracting) shortened the period of the cycle. Stimulation during the returnstroke prolonged the cycle. Changes in cycle period were accompanied by in-phase adjustments of the EMG burst duration or interburst interval which was being expressed at the time of stimulus delivery. The in-phase adjustment of each muscle served to maintain the timing relationships between muscles, and resulted in the preservation of the intracycle motor pattern. Cutaneous and muscle-nerve stimulation had dramatically different effects on the locomotor rhythm. Cutaneous nerve stimulation produced period changes in poststimulus cycles which led to a temporary phase shift of the swimming rhythm. This temporary modulation suggests that cutaneous afferents do not have direct access to the timing circuitry of the central nervous system locomotor network. Muscle-nerve stimulation only altered the period of the cycle in progress at the time of stimulus delivery, and thus permanently reset the locomotor rhythm. This permanent phase shift suggests that muscle afferents have direct access to a central timing network which controls the locomotor rhythm.

Afferent Pathways↗