Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2025
Early peripheral nerve impairments in type 1 diabetes are associated with cortical inhibition of ankle joint proprioceptive afference.
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Mujunen Toni, Sompa Urho, Muñoz-Ruiz Miguel, Monto Elina, Rissanen Valtteri, Ruuskanen Heli, Ahtiainen Petteri, Piitulainen Harri
Аннотация
OBJECTIVE: Diabetic sensorimotor peripheral neuropathy (DSPN) is a common complication of type 1 diabetes mellitus (T1DM). However, it is still unclear how the cortical processing of proprioceptive afference is altered due to DSPN.
METHODS: Cortical responses to right and left ankle joint rotations were recorded with magnetoencephalography and pooled together in 20 T1DM participants and 20 healthy controls for source space comparisons. T1DM participants also underwent a lower limb nerve-conduction study to correlate peripheral nerve function with the cortical responses.
RESULTS: Primary sensorimotor (SM1) cortex activation was wider in T1DM patients during beta suppression, with no between-group differences in the response strength. However, stronger beta suppressions in T1DM patients were correlated with axon-loss in the peripheral sensory afferents (p < 0.05). Weaker beta rebounds and stronger SM1 evoked field amplitudes were associated with impaired conduction velocities in the mixed nerves (p < 0.05). Lastly, stronger SM1 beta power was associated with both demyelination and axon-loss in the lower limb sensory afferents (p < 0.05).
CONCLUSIONS: T1DM is accompanied with wider SM1 cortex activation to proprioceptive stimuli, and the early asymptomatic DSPN impairments are linked to increased levels of cortical inhibition.
SIGNIFICANCE: T1DM is associated with comprehensive central pathophysiology evident in early DSPN.
METHODS: Cortical responses to right and left ankle joint rotations were recorded with magnetoencephalography and pooled together in 20 T1DM participants and 20 healthy controls for source space comparisons. T1DM participants also underwent a lower limb nerve-conduction study to correlate peripheral nerve function with the cortical responses.
RESULTS: Primary sensorimotor (SM1) cortex activation was wider in T1DM patients during beta suppression, with no between-group differences in the response strength. However, stronger beta suppressions in T1DM patients were correlated with axon-loss in the peripheral sensory afferents (p < 0.05). Weaker beta rebounds and stronger SM1 evoked field amplitudes were associated with impaired conduction velocities in the mixed nerves (p < 0.05). Lastly, stronger SM1 beta power was associated with both demyelination and axon-loss in the lower limb sensory afferents (p < 0.05).
CONCLUSIONS: T1DM is accompanied with wider SM1 cortex activation to proprioceptive stimuli, and the early asymptomatic DSPN impairments are linked to increased levels of cortical inhibition.
SIGNIFICANCE: T1DM is associated with comprehensive central pathophysiology evident in early DSPN.