Clinical Identification of the Vertebral Level at Which the Lumbar Sympathetic Ganglia Aggregate

BACKGROUND: The location and the number of lumbar sympathetic ganglia (LSG) vary between individuals. The aim of this study was to determine the appropriate level for a lumbar sympathetic ganglion block (LSGB), corresponding to the level at which the LSG principally aggregate. METHODS: Seventy-four consecutive subjects, including 31 women and 31 men, underwent LSGB either on the left (n = 31) or the right side (n = 43). The primary site of needle entry was randomly selected at the L3 or L4 vertebra. A total of less than 1 ml of radio opaque dye with 4% lidocaine was injected, taking caution not to traverse beyond the level of one vertebral body. The procedure was considered responsive when the skin temperature increased by more than 1℃ within 5 minutes. RESULTS: The median responsive level was significantly different between the left (lower third of the L4 body) and right (lower margin of the L3 body) sides (P = 0.021). However, there was no significant difference in the values between men and women. The overall median responsive level was the upper third of the L4 body. The mean responsive level did not correlate with height or BMI. There were no complications on short-term follow-up. CONCLUSIONS: Selection of the primary target in the left lower third of the L4 vertebral body and the right lower margin of the L3 vertebral body may reduce the number of needle insertions and the volume of agents used in conventional or neurolytic LSGB and radiofrequency thermocoagulation.

Replication of the Association between Copy Number Variation on 8p23.1 and Autism by Using ASD-specific BAC Array

To discover genetic markers for autism spectrum disorder (ASD), we previously applied genome-wide BAC array comparative genomic hybridization (array-CGH) to 28 autistic patients and 62 normal controls in Korean population, and identified that chromosomal losses on 8p23.1 and on 17p11.2 are significantly associated with autism. In this study, we developed an 8.5K ASD-specific BAC array covering 27 previously reported ASD-associated CNV loci including ours and examined whether the associations would be replicated in 8 ASD patient cell lines of four different ethnic groups and 10 Korean normal controls. As a result, a CNV-loss on 8p23.1 was found to be significantly more frequent in patients regardless of ethnicity (p<0.0001). This CNV region contains two coding genes, DEFA1 and DEFA3, which are members of DEFENSIN gene family. Two other CNVs on 17p11.2 and Xp22.31 were also distributed differently between ASDs and controls, but not significant (p=0.069 and 0.092, respectively). All the other loci did not show significant association. When these evidences are considered, the association between ASD and CNV of DEFENSIN gene seems worthy of further exploration to elucidate the pathogenesis of ASD. Validation studies with a larger sample size will be required to verify its biological implication.