This study was designed to examine the behaviorial immunohistochemical changes of spinal glial cells and spinal Interleukin (IL)-1β expression after various nerve root injuries used as models of lumbar radiculopathy. In order to better understand the role of central inflammation in the pathophysiologic mechanisms that give rise to pain associated with lumbar radiculopathy, this research studied the relationship between pain-related behavior associated with spinal glial activation and IL-1β expression generated by three types of nerve root injury: loose ligation with chromic gut, loose ligation with silk, and tight ligation with silk. An animal model of lumbar radiculopathy originally described by Kawakami and Weinstein involved loose ligation of unilateral L4–L6 nerve roots with chromic gut. Characterization and establishment of such an animal model of low back pain enables further investigation of the nature of the pathophysiologic mechanisms associated with lumbar radiculopathy in humans. Seventy-three rats were divided into four treatment groups. Chromic group (n = 25): The L5 nerve roots (dorsal and ventral) were exposed by hemilaminectomy and loosely ligated with chromic gut. Tight silk group (n = 18): The exposed L5 nerve roots were tightly ligated extradurally with 5-0 silk suture. Loose silk group (n = 15): two loose ligatures of 5-0 silk were placed around the exposed L5 nerve roots. Sham group (n = 15): the rats were subjected to laminectomy alone for exposing nerve roots. Following surgery, thermal hyperalgesia and mechanical allodynia was assessed time-dependently up to 42 days post operatively. At 1, 3, 7, 14, and 42 days postoperatively, the rats in each group were perfused with fixative. The L5 spinal cord segments was harvested and cryosectioned for glial and cytokine immunohistochemistry. In the chromic and the tight silk group, an immediate and sustained mechanical allodynia was observed in the ipsilateral hind paw up to 35 days postoperatively. The loose silk group also showed an immediate mechanical allodynia that subsided by 14 days postoperatively. Sham-treated animals exhibited mild mechanicalallodynia for the initial 7 days after the surgery. Thermalhyperalgesia was evident in the three primary treatment groups, but not in the sham-treated rats. OX-42 expression was elevated in the gray matter of the L5 spinal section by 3 days in the chromic, the tight silk, and the loose silk groups as compared to the sham group. Astrocytic activation increased over time in all groups except the sham group. There was no direct correlation between degree of microglial response and severity of pain behaviors. In contrast, astrocytic activation demonstrated a direct relationship with the elevation of mechanical allodynia for the first 7 days. In addition, spinal IL-1β protein expression was increased bilaterally in the superficial layer of the dorsal horn and cell nuclei of the ventral horns in the ligature treated groups as compared with the sham group. Direct mechanical and/or chemical injury to lumbar roots in the rat gives rise to pain behavior suggestive of lumbar radiculopathy. The finding that glial activation and enhanced IL-1β expression are observed in the spinal cord after root injury supports a central, neuroimmune component in the generation of lumbar radiculopathy. A further understanding of the immunologic consequences of root injury may lead to further development and the novel use of selective cytokine–inflammatory inhibitors for the treatment of low back pain associated with radiculopathy.

This study was designed to assess both lumbar sagittal balance and clinical outcomes of decompression and posterolateral fusion for degenerative lumbar spondylolisthesis. As an index for the radiologic evaluation of sagittal alignment, the L1 axis S1 distance was used (i.e., the horizontal distance from the plumbline of the center in the L1 to the back corner of the S1). To determine whether lumbar sagittal balance affected the clinical outcome after posterolateral fusion. Little is known about whether the sagittal vertical axis influences clinical outcomes in cases of degenerative lumbar spondylolisthesis. A retrospective review of 47 patients (15 men and 32 women), ranging in age from 41 to 79 years, was conducted. The mean follow-up period was 3.6 years. Relations among outcomes including the visual analog pain scale, recovery rate, L1 axis S1 distance, slippage, and lumbar lordosis were evaluated. Recovery rates were 44% and 62% in patients whose preoperative L1 axis S1 distance, respectively, was more than 35 mm (Group A, n = 16) and less than 35 mm (Group B, n = 31) (P < 0.05). Follow-up assessment found a positive correlation between only lordosis and recovery rate. Severe low back pain and lower recovery rate were observed in patients with in situ fusion in Group A (n = 9), as compared with patients with reduced slippage in Group A (n = 7) and patients in Group B. Both preoperative L1 axis S1 distance and lordosis at follow-up assessment affected surgical outcome. Reduction of slippage may improve clinical outcomes of posterolateral fusion for degenerative lumbar spondylolisthesis with an L1 axis S1 distance more than 35 mm.

Study Design This study was designed to evaluate whether allografts of intervertebral disc materials produce hyperalgesia in the rat and whether an immune response, pH, or chemicals correlate with the induced hyperalgesia. Objective To elucidate the pathomechanisms of radicular pain secondary to lumbar disc herniation. Summary of Background Data It has been reported that a low pH, an autoimmune reaction, or chemical radiculitis is likely responsible for radicular pain associated with lumbar disc herniation. In animal studies, it has been shown that hyperalgesia (an increased sensitivity to painful stimuli) involves activation of phospholipase A₂ and nitric oxide synthase. Methods Fat, nucleus pulposus, and anulus fibrosus were allografted into the epidural space at L6 in the rat. Withdrawal response thresholds to mechanical stimuli and withdrawal response latencies to thermal stimuli on the tail and pH in the applied tissues were measured after surgery. Interleukin-1, phospholipase A₂, and nitric oxide synthase were examined in the applied tissues using immunohistochemistry, nicotineamide adenine dinucleotide phosphate-diaphorase histochemistry, and in situ hybridization. Results Allografted fat did not produce hyperalgesia. Allografts of nucleus pulposus and nucleus pulposus plus anulus fibrosis showed evidence of mechanical and thermal hyperalgesia, respectively. There were no observed changes in pH over time. Although interleukin-1 was demonstrated in all applied tissues, phospholipase A₂ was only observed around the applied nucleus pulposus and nucleus pulposus plus anulus fibrosus. Nitric oxide synthase was only markedly increased around the applied tissues. Conclusion The nucleus pulposus and anulus fibrosus produce different forms of hyperalgesia (mechanical vs. thermal) associated with different and distinct immunohistochemical changes. It is possible that radicular pain of a lumbar disc herniation results from chemicals, such as phospholiapse A₂ and nitric oxide.