Diabetic Neuropathy Influences Control of Spinal Mechanisms.

PURPOSE: Comprehensive evaluation of the upstream sensory processing in diabetic symmetrical polyneuropathy (DSPN) is sparse. The authors investigated the spinal nociceptive withdrawal reflex and the related elicited somatosensory evoked cortical potentials. They hypothesized that DSPN induces alterations in spinal and supraspinal sensory-motor processing compared with age- and gender-matched healthy controls. METHODS: In this study, 48 patients with type 1 diabetes and DSPN were compared with 21 healthy controls. Perception and reflex thresholds were determined and subjects received electrical stimulations on the plantar site of the foot at three stimulation intensities to evoke a nociceptive withdrawal reflex. Electromyogram and EEG were recorded for analysis. RESULTS: Patients with DSPN had higher perception (P < 0.001) and reflex (P = 0.012) thresholds. Fewer patients completed the recording session compared with healthy controls (34/48 vs. 21/21; P = 0.004). Diabetic symmetrical polyneuropathy reduced the odds ratio of a successful elicited nociceptive withdrawal reflex (odds ratio = 0.045; P = 0.014). Diabetic symmetrical polyneuropathy changed the evoked potentials (F = 2.86; P = 0.025), and post hoc test revealed reduction of amplitude (-3.72 mV; P = 0.021) and prolonged latencies (15.1 ms; P = 0.013) of the N1 peak. CONCLUSIONS: The study revealed that patients with type 1 diabetes and DSPN have significantly changed spinal and supraspinal processing of the somatosensory input. This implies that DSPN induces widespread differences in the central nervous system processing of afferent A-δ and A-ß fiber input. These differences in processing may potentially lead to identification of subgroups with different stages of small fiber neuropathy and ultimately differentiated treatments.

Peripheral, synaptic and central neuronal transmission is affected in type 1 diabetes.

AIMS: We hypothesized that adults with type 1 diabetes and severe polyneuropathy have alterations in neuronal transmission at different anatomical levels. The aims were to investigate upstream sensory neuronal activation in terms of peripheral, spinal, precortical, and cortical transmission. METHODS: 48 participants with type-1 diabetes and polyneuropathy, and 21 age-matched healthy participants were included. Electrophysiological median nerve recordings were used to analyze peripheral transmission at Erb's point (P9-N11); spinal evoked potentials at Cv7 (P11-N14); subcortical evoked potentials at Oz (N14-P18); early cortical evoked potentials at CP5 (N20-P22); late cortical evoked potentials at C1 (N60-P80) and estimated cortical inter-peak latencies as measures of central conduction time. RESULTS: In comparison to healthy, the presence of diabetes prolonged peripheral transmission at P9 and N11 (+0.49 ms, p = .000; +0.47 ms, p = .04, respectively), early cortical evoked potentials at CP5: N20 (+2.41 ms, p = .003) and P22 (+5.88 ms, p = .001) and cortical potentials at C1: N60 (+39.08 ms, p = .001) and P80 (+54.55 ms, p = .000) and central conduction time. Decreased amplitudes were shown peripherally (-2.13 µV, p = .000), spinally (-0.57 µV, p = .005) and pre-cortically (-0.22 µV, p = .004). In both healthy and people with diabetes increased central conduction time were associated with decreased parasympathetic tone (ρ = -0.52, p = .027; ρ = -0.35, p = .047, respectively). CONCLUSION: Neuronal afferent transmission and brain responses were significantly impaired in diabetes and the presence of prolonged central conduction time is indicative of severe extensive neuronal damage. Trial registry number: EUDRA CT: 2013-004375-12; clinicaltrials.gov: NCT02138045.