Introduction

Low-back pain (LBP) is complex and a prominent health care issue at all Health-care levels.1 Pathophysiology of lower-back and limb pain may include nociceptive back pain, somatic referred pain, radicular pain (RP), and radiculopathy 2. The latter two are considered neuropathic-pain (NeP) conditions3. Radiculopathy is the result of a conduction block along a spinal nerve or its roots while RP is the expression of abnormal neuronal singling arising from an injured dorsal root, its ganglion3, or inflamed nerve 4–6. Nociceptive back pain is due to lumbar-spine nociceptors activation. In contrast, the convergence of activated nociceptive afferents on the spinal-cord second-order neurons which subtend regions of the lower limb cause somatic referred pain.
Clinically, RP and radiculopathy show neurological signs and symptoms3. RP may show dysesthesias, whereas radiculopathy may show paresthesias and negative signs like compromised reflexes, numbness, and weakness depending on whether sensory or motor fibers are involved, respectively.
Differential diagnosis of LBP pain, and hence congruent therapeutic approach, are challenging as clinical presentation patterns are variable and different pathophysiological elements may coexist. A focused history, thorough clinical and neurological examination may guide differential diagnosis and treatment 1. Anticonvulsants, such as gabapentin or pregabalin, along with antidepressants, are considered the first choice or bridge therapy for non-invasive treatment of RP 7–9.
We have previously reported the description and reliability features of a clinical adjunctive test, namely, the Buttock Applied Strain (BUAS) test, that may facilitate the differential diagnosis of LBP and may uncover the presence of RP in LBP patients 10. This test showed high sensitivity, specificity and, linear correlation with the PainDETECT (PD) questionnaire and thus implying the ability to detect the presence of NeP (ie, lumbar-RP) in LBP patients.
To further support the BUAS-test diagnostic ability, we sought to verify the influence of an anticonvulsant (namely, gabapentin) on PD outcomes and pain scores of patients who were positive to the BUAS test and hence diagnosed with potential lumbar-RP. The latter patients are routinely treated in our practice with the gabapentin protocol. We have hypothesized that, given the properties of gabapentin to modulate NeP (and hence lumbar-RP), a subsequent significant clinical improvement in PD outcomes and pain scores, might be considered a piece ofex-adiuvantibus evidence for the ability of the BUAS test to detect lumbar-RP.