Spinal Cord Stimulation Eases Decades-Old Nerve Pain After Spinal Injury

For more than thirty years, a Croatian man lived with severe neuropathic pain that traced back to a single moment in 1991, when a gunshot wound to his spine left him with permanent neurological damage. The pain never fully responded to physical therapy, rehabilitation, or a long list of medications from a specialized pain clinic. By the time he was referred to Dubrava University Hospital in Zagreb in 2024, at the age of 60, his pain had worsened and his daily functioning was deteriorating further. What happened next is now the subject of a case report published in Frontiers in Pain Research: surgeons implanted a spinal cord stimulation device, and within two years his pain had fallen from a rating of 8 out of 10 to 2 out of 10, his disability scores had improved dramatically, and he had stopped taking every medication he had been using to control the pain.

The case is striking not simply because the treatment worked, but because of how long the pain had been established. Neuropathic pain after spinal cord injury affects roughly half of all people living with such injuries, and it is among the most disabling consequences of the condition, undermining rehabilitation, psychological health, and quality of life. When pain persists for decades, the nervous system undergoes lasting changes in how it processes nociceptive signals, and many clinicians have assumed that such deeply entrenched pain becomes progressively harder to treat. The new report challenges that assumption, at least for one carefully selected patient, by showing a sustained, multidimensional response to neuromodulation more than three decades after the original injury.

The patient’s history was complex. The 1991 gunshot injury left metallic fragments lodged at the T12–L1 level of his spine, and he developed bilateral spastic paraparesis, meaning weakness and stiffness in both legs, markedly worse on the left side, along with muscle atrophy in his left lower limb and persistent sensory disturbances. Because no complete contemporary neurological examination following the standardized ISNCSCI framework was available from the time of injury, the clinical team could not reliably reconstruct a formal neurological level of injury or an AIS severity grade. Nevertheless, the pattern of his pain, burning and dysesthetic sensations across both lower extremities and the lower back, was clinically consistent with below-level neuropathic pain arising from the spinal cord injury itself.

Before recommending stimulation, the team worked to exclude other explanations. Electrodiagnostic testing found no evidence of peripheral neuropathy, and the patient had no history of diabetes. A lumbar CT scan showed no disc herniation or spinal canal stenosis that would require surgery, ruling out a mechanically correctable lesion that might account for his symptoms. Magnetic resonance imaging was impossible because of the retained bullet fragments. With a predominantly neuropathic pain phenotype, failure of prolonged conservative management, and no surgical target, the multidisciplinary team concluded that the pain was attributable to the old spinal cord injury and was refractory to further conservative treatment, making him a candidate for spinal cord stimulation.

The surgery itself was performed on February 15, 2024, under local anesthesia with the patient lying prone, which allowed the surgeons to test stimulation intraoperatively while the patient reported on coverage of his painful areas. Under fluoroscopic guidance, two epidural leads were positioned at the T8–T9 vertebral level, one slightly above the other, and connected to a Medtronic Inceptiv implantable pulse generator placed under the skin of the left gluteal region. The primary stimulation mode was differential target multiplexed, or DTM, stimulation, a paradigm designed to modulate pain-processing circuits with complex, interleaved signal patterns, supplemented by an individualized conventional tonic program and, later in follow-up, the device’s closed-loop stimulation function, which adjusts output in real time based on evoked compound action potentials recorded from the spinal cord.

The results were rapid and, so far, durable. About two months after implantation, the patient reported pain ranging from 0 to 2 out of 10, and by that point he had already discontinued pregabalin, duloxetine, clonazepam, and etoricoxib, the medications that had formed his pain regimen. At the formal 12-month assessment, his Visual Analog Scale score had fallen from 8 to 3, his Oswestry Disability Index had dropped from 60 percent to 30 percent, and his DN4 score, a screening measure of neuropathic pain features, had fallen from 8 to 2. His self-rated health on the EQ-VAS scale climbed from 40 out of 100 to 75, and his Hospital Anxiety and Depression Scale scores fell from 10 for both anxiety and depression to 3 and 4 respectively.

By 24 months, the gains had been maintained or extended. Pain intensity fell further to 2 out of 10, disability improved to an Oswestry score of 20 percent, self-rated health reached 80 out of 100, and the anxiety and depression scores declined to 2 and 3. The patient remained free of pain-directed medication, using occasional analgesics only for unrelated complaints such as headaches. He reported subjectively that his overall pain had decreased by more than 70 percent compared with his preoperative state, and he remained physically active. Residual burning pain in his feet and lower legs, particularly in the evenings, was managed through individualized reprogramming of the device. Crucially, no neurological deterioration, infection, lead migration, or other device-related complication occurred across the entire two-year follow-up period.

Why might stimulation still work after so many years of pain? The classical explanation for spinal cord stimulation is the gate-control model: activating large-diameter sensory fibers in the dorsal columns suppresses nociceptive transmission in the dorsal horn of the spinal cord. But contemporary research paints a far richer picture. Stimulation appears to modulate excitatory and inhibitory neurotransmission, alter dorsal horn neuronal activity, influence glial and neuroimmune signaling, and engage both ascending pain pathways and descending inhibitory systems that reach deep into supraspinal networks governing the sensory and emotional dimensions of pain. This distributed mechanism offers a plausible framework for why the patient’s improvements extended beyond pain intensity to psychological well-being and perceived health, although the authors are careful to note that a single case cannot establish mechanism.

The authors also place their observation in sobering context. A recent systematic review of spinal cord stimulation for pain after spinal cord injury identified only ten eligible studies comprising 43 patients, consisting mostly of case reports and small series with substantial heterogeneity in injury type, stimulation parameters, and outcome reporting. The certainty of that evidence is low, and favorable outcomes may be inflated by selection and publication bias. A meta-regression of stimulation outcomes found that longer pain duration was associated with reduced relief in univariable analysis, although no factor remained independently predictive in multivariable modeling. The Zagreb team therefore does not claim that chronicity is irrelevant to patient selection, only that very long pain duration does not invariably eliminate the capacity for a meaningful response.

The report carries clear limitations that the authors acknowledge candidly. Causal inference is impossible in a single patient, and some improvement could reflect nonspecific treatment effects or unmeasured factors. The Oswestry Disability Index is not validated specifically for spinal cord injury populations, so its improvement should be read as reduced pain-related disability rather than neurological recovery, and the patient’s fixed spastic paraparesis was unchanged throughout. The DN4 is a screening tool, not a quantitative measure of treatment response. Still, the case expands a very thin evidence base and suggests that symptom duration should be investigated as a modifier, rather than an absolute barrier, to neuromodulation in spinal cord injury pain. For the patient himself, the outcome was unambiguous: sustained relief, restored activity, freedom from daily medication, and, in his own assessment, a highly satisfactory result that endured through two full years of follow-up.

Subject of Research: Spinal cord stimulation for decades-old neuropathic pain after traumatic spinal cord injury

Article Title: Case Report: Beyond chronicity: sustained multidimensional response to spinal cord stimulation three decades after traumatic spinal cord injury

Article References: Case Report: Beyond chronicity: sustained multidimensional response to spinal cord stimulation three decades after traumatic spinal cord injury. (n.d.). https://doi.org/10.3389/fpain.2026.1969355

Image Credits: AI Generated

DOI: 10.3389/fpain.2026.1969355

Keywords: spinal cord stimulation, neuropathic pain, spinal cord injury, neuromodulation, chronic pain, case report, DTM stimulation, closed-loop stimulation, pain management, neurosurgery, disability, rehabilitation