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Peripheral neuropathy is the most common long-term complication in diabetes and is involved in changes in diabetic gait and posture. The regression of nerve function leads to various deficits in the sensory and motor systems, impairing afferent and efferent pathways in the lower extremities. This study aimed to examine how reduced plantar-afferent feedback impacts the gait pattern. Cutaneous sensation in the soles of both feet was experimentally reduced by means of intradermal injections of an anaesthetic solution, without affecting foot proprioception or muscles. Ten subjects performed level walking at a controlled velocity before and after plantar anaesthesia. Muscle activity of five leg-muscles, co-contraction ratios for the knee and ankle joint, ground reaction forces (GRF), spatiotemporal characteristics, joint angles and moments of the hip, knee and ankle were analysed. The intervention significantly lowered plantar sensation, reducing it to the level of sensory neuropathy. Spatiotemporal gait characteristics remained unchanged. The ankle joint was more dorsiflexed which coincided with increased tibialis anterior and decreased gastrocnemius medialis muscle activity during foot flat to mid-stance. In addition, the knee joint was more flexed accompanied by increased biceps femoris activity and higher internal knee-extension moment. With regard to gait dynamics, a delay of the first peak of the vertical GRF was observed. Increased soleus and tibialis anterior muscle activity were found during the end of stance. Short-term loss of plantar sensation affects lower-limb kinematics and gait dynamics, particularly during the first half of stance, and contributes to modified muscle-activation patterns during locomotion.

Small iontophoretic ejections of horseradish peroxidase (HRP) were made from recording-multibarrel micropipette assemblies in areas of the cat's suprageniculate nucleus (SGn) that contained visually responsive neurones. The sources of afferents of the SGn were determined by locating the labeled cell bodies of neurones that were presumed to send their axons to the area of the SGn containing the light-sensitive cells. The greatest concentration of labeled cell bodies was found in the granular insular cortex and the adjacent area of agranular insula. Most cells projecting to SGn from these areas were distributed in the middle and lower laminae. A second intensely labeled region was found in stratum opticum and stratum griseum intermediate of the superior colliculus. Other areas containing labeled cells that were distributed with intermediate density included the ventral thalamic nuclear complex (basal, medial, and lateral divisions), periaqueductal gray (PAG), zona incerta, and pretectal nuclei (posterior, medial, and anterior divisions). Sparsely labeled sites included the fields of Forel, substantia nigra (pars reticulata), peri-insular cortex, superior colliculus (profundum), lateral suprasylvian cortex (posterolateral lateral suprasylvian, PLLS and posteromedial lateral suprasylvian, PMLS), anterior ectosylvian cortex, thalamic reticular complex, nucleus of the optic tract, basal part of the ventromedial hypothalamic nucleus, and the pontine reticular nucleus (oralis) and adjacent reticular formation. Together with previous electrophysiological and neuroanatomical studies, the findings suggest that the SGn provides an integrating link between limbic structures and certain modalities of sensory information.

We conclude that recording evoked acceleromyographic responses at the trapezius muscle is an acceptable alternative when monitoring from the adductor pollicis muscle is compromised. Nevertheless, we caution that recording a 90% TOF response at the trapezius muscle may overestimate functional recovery from the neuromuscular blockade. This trial was registered at ClinicalTrials.gov identifier, NCT01849198.

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