Treatment of central pain syndrome with spinal cord stimulation

Central pain syndrome (CPS) is a neurological disorder caused by damage or dysfunction of the central nervous system. Both conservative and operative methods of treatment are used in its treatment, but in most cases their effectiveness is rather low. We are presenting the clinical observation of a 60-year-old patient with spinal cord injury at the level of Th10 due to a car accident that occurred 44 years before the treatment in our clinic, who suffered from phantom pain that occurred after bilateral above the knee amputation because of advanced peripheral vascular disease. Due to the ineffectiveness of the conservative treatment, it was decided to proceed with spinal cord stimulation. The presence of pronounced postoperative changes in the area of spinal cord injury has complicated the transcutaneous placement of trial leads at the L1-L2 and Th12-L1 level. We managed to introduce leads at the level of Th7-Th8 and position them at the level of Th5-Th7. During continuous neurostimulation the pain in the sacrum, in the area of the hip joints, the phantom pain was relieved. The patient stopped using all pain medications. Spinal cord stimulation can be utilized as an alternative treatment for patients with intractable CPS.

Aromatase Inhibition Exacerbates Pain and Reactive Gliosis in the Dorsal Horn of the Spinal Cord of Female Rats Caused by Spinothalamic Tract Injury

Central pain syndrome is characterized by severe and excruciating pain resulting from a lesion in the central nervous system. Previous studies have shown that estradiol decreases pain and that inhibitors of the enzyme aromatase, which synthesizes estradiol from aromatizable androgens, increases pain sensitivity. In this study we have assessed whether aromatase expression in the dorsal horns of the spinal cord is altered in a rat model of central pain syndrome, induced by the unilateral electrolytic lesion of the spinothalamic tract. Protein and mRNA levels of aromatase, as well as the protein and mRNA levels of estrogen receptors α and β, were increased in the dorsal horn of female rats after spinothalamic tract injury, suggesting that the injury increased estradiol synthesis and signaling in the dorsal horn. To determine whether the increased aromatase expression in this pain model may participate in the control of pain, mechanical allodynia thresholds were determined in both hind paws after the intrathecal administration of letrozole, an aromatase inhibitor. Aromatase inhibition enhanced mechanical allodynia in both hind paws. Because estradiol is known to regulate gliosis we assessed whether the spinothalamic tract injury and aromatase inhibition regulated gliosis in the dorsal horn. The proportion of microglia with a reactive phenotype and the number of glial fibrillary acidic protein–immunoreactive astrocytes were increased by the injury in the dorsal horn. Aromatase inhibition enhanced the effect of the injury on gliosis. Furthermore, a significant a positive correlation of mechanical allodynia and gliosis in the dorsal horn was detected. These findings suggest that aromatase is up-regulated in the dorsal horn in a model of central pain syndrome and that aromatase activity in the spinal cord reduces mechanical allodynia by controlling reactive gliosis in the dorsal horn.