Chapter Clinical Summary
Academic synthesis, diagnostic methodology, and surgical recommendationsSpinal pain represents one of the leading global causes of disability, healthcare consultation, and work absenteeism. Understanding its mechanisms has expanded substantially beyond the classic model of mechanical spinal tissue injury. Acute pain typically acts as a physiological warning signal of tissue damage, whereas chronic pain often involves peripheral sensitization, central sensitization, neural plasticity, and cognitive-affective influences. In this setting, pain ceases to be merely a symptom and can become the disease process itself. Management requires differentiating nociceptive, neuropathic, and nociplastic pain mechanisms to guide rational pharmacotherapy, physical rehabilitation, interventional procedures, and behavioral therapies, avoiding excessive reliance on long-term opioids and unnecessary surgical interventions.
To present the neurobiological foundations of acute and chronic spinal pain and guide the clinical differentiation of nociceptive, neuropathic, and nociplastic mechanisms. The reader will learn to structure multimodal conservative treatment, select targeted pharmacological agents, identify indications for interventional blocks and radiofrequency, recognize psychological yellow flags, and implement multidisciplinary rehabilitation strategies.
Pain is categorized into nociceptive (tissue/inflammatory), neuropathic (somatosensory lesion/disease, such as radiculopathy), and nociplastic (altered nociceptive processing without clear tissue damage, such as fibromyalgia or non-specific central back pain). Central sensitization is characterized by hyperalgesia, allodynia, and temporal summation, requiring distinct therapeutic strategies.
Acute pain focuses on self-care, activity modification (avoiding bed rest), physical therapy, and short-term analgesics (NSAIDs, acetaminophen, muscle relaxants). In chronic pain, active exercise-based physical rehabilitation, functional restoration, and cognitive behavioral therapy are first-line interventions.
First-line agents for neuropathic/sensitized pain include gabapentinoids (gabapentin, pregabalin), SNRIs (duloxetine), and tricyclic antidepressants. Long-term opioid therapy is discouraged due to tolerance, hyperalgesia, dependency risk, and lack of long-term functional improvement.
Image-guided facet injections, medial branch blocks, radiofrequency neurotomy, and transforaminal epidural injections provide diagnostic confirmation and therapeutic analgesia. In refractory chronic neuropathic pain (e.g., failed back surgery syndrome), spinal cord stimulation (SCS) and dorsal root ganglion (DRG) stimulation offer evidence-based symptomatic relief.
When evaluating a patient with spine pain, determining the predominant mechanism (nociceptive, neuropathic, or nociplastic) guides therapy. Prescribing standard anti-inflammatory drugs or surgery for nociplastic pain is ineffective and harmful. Neuropathic radicular pain responds best to gabapentinoids/SNRIs and epidural injections. Facet-mediated axial pain is confirmed by diagnostic medial branch blocks before considering radiofrequency neurotomy. Biopsychosocial yellow flags must be addressed through active rehabilitation and psychological support.