Quantitative discometry: Low-dose concordant pain onset identifies sensitized annular nociceptors under pressure-volume-controlled provocation.

Background: Provocative discography is controversial because it couples mechanically induced disc stimulation to a subjective pain report and is often interpreted as a simple yes/no test of "discogenic pain." Pressure-volume-controlled discography ("discometry") allows disc provocation to be treated as a dose-response experiment using static pressure above opening (ΔP) and cumulative mechanical work (W), rather than pressure alone. Objective: To determine whether discs that reproduce a patient's concordant pain under pressure-volume control exhibit a distinct low-dose onset phenotype compared with discs that never declare, and to interpret these patterns in the context of annular versus vertebrogenic pain mechanisms. Methods: We retrospectively analyzed pressure-volume-controlled lumbar discography from a single outpatient spine practice. Discs were injected in fixed volume increments with static plateau pressures recorded at each step under protocol caps (ΔP ≤ 50 psi above opening; volume ≤3.5 mL). For each disc, we identified either the onset event (first 0.5 mL step with definite concordant pain ≥4/10, sustained ≥30 s) or a final-negative (censored) event if no onset occurred under the caps (i.e., the disc "never declared"). Static ΔP at the event (ΔP_event) and cumulative mechanical work (W_event = Σ ΔP × ΔV) were calculated, and an energy-equivalent stiffness (K_eq = 2W/V Results: Structurally abnormal discs that reproduced the presenting pain almost always did so at relatively low ΔP_event and W_event, yet with moderate-to-severe pain intensity at onset. Discs that never declared under the same protocol caps tolerated substantially higher ΔP_event and W_event, and morphologically normal discs clustered at the extreme of high-dose tolerance with rare positive responses. This separation between low-dose onset and high-dose tolerance persisted within fissured and disrupted strata, within encounters (positive vs negative discs in the same patient), and after stiffness normalization using K_eq, arguing against generalized "softness" as the sole explanation. In a subset with complete step-index data, most onset-positive discs declared by approximately 1.7 mL of injected volume and nearly all by 1.7-2.2 mL under slow, staged injection. Conclusion: These findings support a reproducible low-dose, high-intensity concordant pain phenotype in structurally abnormal discs, most consistent with chemically and mechanically sensitized nociceptors in the annulus and at the annulus-endplate junction. Other discs-whether morphologically normal or with more prominent vertebrogenic features-remain load-tolerant under bounded pressurization, suggesting different dominant generators. In this framework, pressure-controlled discography functions less as a binary test and more as a quantitative phenotyping tool that uses combined pressure and work thresholds to distinguish annular-/junctional-dominant low-dose responses from higher-dose, load-tolerant patterns, and may help refine patient selection for disc-directed versus vertebrogenic-targeted interventions in future prospective studies.