A punctate midline myelotomy performed in a patient effectively eliminated residual, intractable pelvic pain, which remained after resolution of uterine cervical cancer. The authors describe the case history of the patient, in whom pain assessments were made, and a surgical procedure performed. Despite large doses of opiate analgesic medications, the patient experienced constant pressure pain in the right lower pelvis, with excruciating pain on bowel movement. Severe weight loss necessitated better pain control. A minimally invasive surgical procedure, a 5-mm deep puncture using a 16-gauge needle on either side of the median septum in the dorsal column of the spinal cord (T-8), resulted in no new neurological deficits. Narcotic medication was tapered, no pain was reported, and the patient resumed daily household activity. Midline myelotomy has typically been performed with the intention of eliminating the crossing fibers of the spinothalamic tract in the anterior white matter commissure. The punctate midline myelotomy described here was performed with the specific intention of interrupting a newly described visceral pain pathway that ascends to higher brain centers through the midline of the dorsal column. The effectiveness of the pain relief seen in this patient suggests that visceral pain of the pelvis in humans may be transmitted in the midline of the dorsal column, as has been recently reported in studies using rats. The effectiveness of the punctate midline myelotomy performed in this one case of pelvic visceral pain suggests that the surgery may eventually be effective in greatly reducing or replacing opiate narcotic medication for visceral pain management.

Withdrawal responses to mechanical and thermal stimuli applied to the plantar surface of the hindpaw were measured before and after bone damage. In separate groups of rats the bone was injured by scraping the periosteum of the tibia, drilling a hole through the tibia, aspirating bone marrow, or drilling a hole through the calcaneus. Scraping the periosteum did not alter withdrawal responses to the mechanical stimuli, or evoke nocifensive behavior. In contrast, secondary mechanical hyperalgesia and allodynia, and cold allodynia were observed after a hole was drilled through the tibia or calcaneus and after aspiration of bone marrow. The secondary hyperalgesia peaked at 2 h after injury. Drilling a hole through the calcaneus permitted primary hyperalgesia to be easily quantified. Primary hyperalgesia lasted up to 24 h after injury. Nocifensive behavior characterized by a lifting and guarding of the damaged limb was also observed after a hole was drilled through the tibia or calcaneus. Drilling a hole through the tibia or calcaneus should be a useful experimental model for investigating the mechanisms underlying bone pain.

Withdrawal reflex responses to graded von Frey filaments applied to the plantar surface of the paw were measured before and after bone hole damage in rats with either a dorsal column (DC) lesion or a sham DC lesion. Two methods were employed to produce models of osteotomy; a small hole was drilled through either the (1) tibia or (2) calcaneus (Houghton, A.K., Hewitt, E. and Westlund, K.N., Enhanced withdrawal responses to mechanical and thermal stimuli after bone injury, Pain, 73 (1997) 325-337). In the rats with a sham DC lesion, a hole through the tibia or calcaneus resulted in the development of mechanical hyperalgesia and allodynia which peaked at 2.5 h. Nocifensive behavior, characterized by a lifting and guarding of the damaged limb, was also observed in animals with a hole through the calcaneus. In contrast, we found that interrupting the dorsal column pathway with a small mid-line lesion (1 week prior to the osteotomy) prevented the development of both the primary and secondary mechanical hyperalgesia and allodynia but not the guarding of the damaged limb. This study provides evidence that axons in the medial part of the dorsal column are involved in the development of mechanical hyperalgesia and allodynia after bone hole injury.