Long-Term Course to Lumbar Disc Resorption Patients and Predictive Factors Associated with Disc Resorption.

The long-term course to lumbar intervertebral disc herniation (LDH) patients receiving integrative Korean medicine treatment and predictive factors associated with disc resorption were investigated. LDH patients who received integrative Korean medicine treatment from February 2012 to December 2015 and were registered in the "longitudinal project for LDH on MRI" were included. Disc resorption amount was measured 3-dimensionally with disc degeneration and modic change levels on baseline and follow-up MRIs. Patient characteristics, Korean medicine use, pain, symptom recurrence, and satisfaction were assessed through medical records and phone surveys. Of 505 participants, 19 did not show disc resorption, while 486 did. A total of 220 displayed resorption rates of ≥50%. LDH volume at baseline was 1399.82 ± 594.96 mm3, and that on follow-up MRI was 734.37 ± 303.33 mm3, indicating a 47.5% decrease (p < 0.0001). Predictive factors for disc resorption were disc extrusion, Komori migration classification, and LDH amount. Approximately 68.4% did not experience symptom recurrence over the 51.86 ± 19.07-month follow-up, and 90.3% were satisfied with Korean medicine treatment. The majority of LDH patients who improved after integrative Korean medicine treatment showed disc resorption within 1 year with favorable long-term outcomes. Predictive factors for disc resorption should be duly considered for informed decision-making. This trial is registered with ClinicalTrials.gov NCT02841163.

GABA(B) receptor-mediated presynaptic inhibition of glycinergic transmission onto substantia gelatinosa neurons in the rat spinal cord.

The GABA(B) receptor-mediated presynaptic inhibition of glycinergic transmission was studied from young rat substantia gelatinosa (SG) neurons using a conventional whole-cell patch clamp technique. Action potential-dependent glycinergic inhibitory postsynaptic currents (IPSCs) were recorded from SG neurons in the presence of 3 mM kynurenic acid and 10 microM SR95531. In these conditions, baclofen (30 microM), a selective GABA(B) receptor agonist, greatly reduced the amplitude of glycinergic IPSCs and increased the paired-pulse ratio. Such effects were completely blocked by 3 microM CGP55845, a selective GABA(B) receptor antagonist, indicating that the activation of presynaptic GABA(B) receptors decreases glycinergic synaptic transmission. Glycinergic IPSCs were largely dependent on Ca2+ influxes passing through presynaptic N- and P/Q-type Ca2+ channels, and these channels contributed equally to the baclofen-induced inhibition of glycinergic IPSCs. However, the baclofen-induced inhibition of glycinergic IPSCs was not affected by either 100 microM SQ22536, an adenylyl cyclase inhibitor, or 1 mM Ba2+, a G-protein coupled inwardly rectifying K+ channel blocker. During the train stimulation (10 pulses at 20 Hz), which caused a marked synaptic depression of glycinergic IPSCs, baclofen at a 30 microM concentration completely blocked glycinergic synaptic depression, but at a 3 microM concentration it largely preserved glycinergic synaptic depression. Such GABA(B) receptor-mediated dynamic changes in short-term synaptic plasticity of glycinergic transmission onto SG neurons might contribute to the central processing of sensory signals.