Chapter Clinical Summary
Academic synthesis, diagnostic methodology, and surgical recommendationsPerioperative neurological injury is among the most dreaded complications of spine surgery, carrying the potential for permanent motor, sensory, or bowel/bladder deficits. Mechanisms include direct mechanical contusion, compression from hematoma or misplaced implants, excessive traction/distraction, spinal cord ischemia, positioning neuropathy, and reperfusion injury. The chapter details functional spinal cord anatomy, vascular territories (anterior spinal artery vs. posterior arteries), and nerve roots. It differentiates spinal cord syndromes from radiculopathies and reviews peripheral nerve injury grading (Seddon and Sunderland classifications: neuropraxia, axonotmesis, neurotmesis). Diagnosis relies on multimodal intraoperative neuromonitoring, serial postoperative neurological exams, and urgent emergency neuroimaging.
To train the reader to identify risk factors and mechanisms of perioperative neurological deficits, recognize new deficits immediately, and structure diagnostic and therapeutic protocols. It covers positioning nerve injuries, white cord syndrome, C5 motor palsy, and neuroprotective strategies.
Dorsal columns, lateral corticospinal tracts, and spinothalamic tracts determine clinical presentation upon injury. Spinal cord blood supply is precarious at watershed thoracic zones (T4-T8). Nerve roots and peripheral plexuses are exposed to traction and pressure during operative maneuvers and patient positioning.
Injuries divide into central spinal cord syndromes and peripheral radiculopathies. Seddon/Sunderland grading guides prognosis. Deficits may present immediately or develop insidiously over hours, meaning a normal examination in the operating room does not eliminate delayed post-op hematoma risk.
Intraoperative monitoring alerts detect subclinical compromise. Postoperatively, serial physical exams are mandatory. Urgent non-contrast CT verifies screw trajectories and bony impingement; urgent emergency MRI identifies compressive hematomas, cord edema, ischemia, or residual herniation. EMG/NCS evaluates peripheral nerve and root recovery after 3-4 weeks.
White Cord Syndrome refers to sudden motor/sensory deterioration following uneventful cervical or thoracic decompression, showing hyperintense T2 cord edema on MRI, attributed to acute reperfusion injury. C5 palsy is a characteristic complication following cervical decompression (laminoplasty or laminectomy and fusion), causing deltoid/biceps paresis due to root tethering or reperfusion.
Stable, mild neuropraxic deficits without structural compression are managed with hemodynamic support, physical therapy, and observation. Rapidly progressive deficits or identifiable compressive causes (epidural hematoma, hardware breach) mandate emergency surgical revision and decompression within hours to maximize recovery.
A new postoperative neurological deficit is an emergency until a reversible mechanical cause is ruled out. Immediate assessment determines whether the deficit is cord-level, radicular, or peripheral nerve-related. Urgent CT/MRI must be obtained without delay. Prone positioning injuries (brachial plexus stretch, ulnar or lateral femoral cutaneous nerve compression) must be recognized and prevented by proper padding and positioning.