200 Section - Multimodal Management of Complex Neuropathic Pain in a Patient with Traumatic Conus Medullaris Syndrome from T12 Complete Spinal Cord Injury

Tuesday, May 19, 2026

6:00 PM - 7:30 PM PT

Presenting Author/Autor expositor(s)

GM

Griffin Mumby, MD

Resident
University of Alberta
Edmonton, Alberta, Canada

Co-Author(s)

HK

Hardeep Kainth, MD

Associate Clinical Professor
University of Alberta
Edmonton, Alberta, Canada

Case Diagnosis: Neuropathic pain (NP) after spinal cord injury (SCI) is common and debilitating, affecting 50-70% of patients. However, adequate pain control is often difficult to achieve due to complex pathophysiologic mechanisms and variable pain phenotypes.

We present a case of a 50-year-old male with a history of traumatic conus medullaris syndrome (T12 complete SCI) seen at our multidisciplinary rehabilitation center. He developed severe bilateral L1/L2 dermatomal and scrotal NP and allodynia, left-sided Meralgia Paresthetica, bilateral adductor spasticity, and central pain impacting sleep, participation in therapy, and daily functioning.

Case Description:

Conservative measures included desensitization, Transcutaneous Electrical Nerve Stimulation, Functional Electrical Stimulation exercises, stress management, and mental health support. Gabapentin, TCAs, and SNRIs only modestly improved symptoms. Anti-convulsants, cannabinoids, and low-potency opioids were trialled as adjuncts, but discontinued due to adverse effects or limited efficacy.

We formulated a successful pain treatment strategy by diagnosing and treating each source of pain. Subcutaneous botulinum toxin significantly reduced L1/L2 dermatomal pain and allodynia. Bupivacaine and lidocaine nerve blocks improved Meralgia Paresthetica by 70%. Bilateral adductor spasticity resolved with botulinum toxin. Central pain improved with pregabalin, and scrotal allodynia with desipramine. An 8-electrode array epidural spinal cord stimulator was implanted 18 months post-injury for residual NP, and later revised to a 32-electrode array, resulting in significant symptom improvement, reduced polypharmacy, and improved daily function.

Discussions:

This case report highlights the complexity of SCI-related NP and the various approaches needed to manage it. Multiple mechanisms, including neuroanatomical alterations, changes in endogenous pain signalling, neuroinflammatory processes, and psychosocial factors, all contribute to a patient’s pain presentation following SCI. As such, treatment should be individualized and multimodal, utilizing conservative, pharmacologic, interventional, and surgical measures when indicated.

Conclusions: NP following SCI can be debilitating and difficult to control. Effective management requires accurate identification of pain phenotypes, multimodal approaches, and individualized treatment strategies.