Case 1: Cervical Syringomyelia & Anterior White Commissure Decussation
Syringomyelia is characterized by a fluid-filled cavity (syrinx) within the central canal of the spinal cord that first compresses the decussating fibers of the spinothalamic tract in the anterior white commissure, producing bilateral, dissociated loss of pain and temperature sensation in a cape-like distribution.
- Clinical recognition: The patient presents with painless burn injuries and bilateral loss of pain and temperature sensation in the upper extremities and upper torso with preserved light touch, vibration, and joint position sense (dissociated sensory loss), typical of syringomyelia (often associated with Arnold-Chiari type I malformation).
- Anatomical pathway: Second-order sensory neurons of the spinothalamic tract originate in the dorsal horn, cross the midline via the anterior white commissure 1 to 2 segments above their entry level, and ascend to the ventral posterolateral (VPL) nucleus of the thalamus.
- Lesion pathophysiology: Because the anterior white commissure lies directly adjacent to the expanding central canal (most commonly in the cervical spinal cord, C8–T1), these decussating spinothalamic fibers are damaged first, leading to symmetric, bilateral loss of pain and thermal sensation limited to the affected spinal levels.
- Syringomyelia damages crossing spinothalamic axons in the anterior white commissure -> bilateral 'cape-like' pain/temperature loss.
- Dorsal columns (vibration and proprioception) ascend uncrossed on the ipsilateral side and are spared in early disease.
