Clinical Course of Motor Deficits from Lumbosacral Radiculopathy Due to Disk Herniation.

BACKGROUND: The clinical course of motor deficits from lumbosacral radiculopathy appears to improve with or without surgery. Strength measurements have been confined to manual muscle testing (MMT) and have not been extensively followed and quantified in prior studies. OBJECTIVE: To determine if motor weakness and patient-reported outcomes related to lumbosacral radiculopathy improve without surgical intervention over the course of 12 months. DESIGN: Prospective observational cohort. SETTING: Outpatient academic spine practice. PARTICIPANTS: Adults with acute radicular weakness due to disk herniation. METHODS: Forty patients with radiculopathy and strength deficit were followed over a 12-month period. Objective strength and performance tests as well as survey-based measurements were collected at baseline and then every 3 months. Patients underwent comprehensive pain management and rehabilitation and/or surgical approaches as determined in coordination with the treating specialist. This study was approved by the institutional review board of Colorado. MAIN OUTCOME MEASUREMENTS: Testing of strength was through MMT, handheld dynamometer, and performance-based testing. Furthermore, visual analog scale, modified Oswestry Disability Index, and 36-Item Short Form Health Survey (SF-36) were used to measure pain and disability outcomes. RESULTS: Of the 40 patients, 33 (82.5%) did not have surgery; 7 (17.5%) had surgery. Twenty-four of the 33 patients (60%) did not undergo surgery and were followed for 12 months (Comprehensive Pain Management and Rehabilitation, Complete [CPM&R-C]), and 9 (22%) did not have surgery and lacked at least one follow-up evaluation (Comprehensive Pain Management and Rehabilitation, Incomplete [CPM&R-I]). No statistically significant differences were found on baseline measures of strength deficits and SF-36 domains between the CPM&R-C, Surgery, and CPM&R-I groups. Pain and disability scores in the Surgery group were significantly higher than in the CPM&R-C at baseline. There were statistically significant improvements in all areas of strength, pain, and function when comparing measurements at the 12-month follow-up to baseline in the CPM&R-C group. CONCLUSIONS: Individuals with motor deficits due to lumbosacral radiculopathy improve over time regardless of treatment choice. Most did not choose surgery, and almost all of these patients regained full strength at 1 year. Strength recovery typically occurred in the first 3 months, but there was ongoing recovery over the course of a year. LEVEL OF EVIDENCE: II.

Androgen regulates brain-derived neurotrophic factor in spinal motoneurons and their target musculature.

Trophic factors maintain motoneuron morphology and function in adulthood. Brain-derived neurotrophic factor (BDNF) interacts with testosterone to maintain dendritic morphology of spinal motoneurons. In addition, testosterone regulates BDNF's receptor (trkB) in motoneurons innervating the quadriceps muscles as well as in motoneurons of the highly androgen-sensitive spinal nucleus of the bulbocavernosus (SNB). Given these interactive effects, we examined whether androgen might also regulate BDNF in quadriceps and SNB motoneurons and their corresponding target musculature. In both motoneuron populations, castration of males reduced BDNF immunolabeling, and this effect was prevented with testosterone replacement. ELISA for BDNF in the target musculature of quadriceps (vastus lateralis, VL) and SNB (bulbocavernosus, BC) motoneurons revealed that BDNF in the VL and BC muscles was also regulated by androgen. However, although castration significantly decreased BDNF concentration in the VL muscle, BDNF concentration in the BC muscle was significantly increased in castrates. Treatment of castrated males with testosterone maintained BDNF levels at those of intact males in both sets of muscles. Together, these results demonstrate that androgens regulate BDNF in both a sexually dimorphic, highly androgen-sensitive neuromuscular system as well as a more typical somatic neuromuscular system. Furthermore, in addition to the regulation of trkB, these studies provide another possible mechanism for the interactive effects of testosterone and BDNF on motoneuron morphology. More importantly, by examining both the motoneurons and the muscles they innervate, these results demonstrate that within a neural system, BDNF levels in different components are differentially affected by androgen manipulation.