Background: We previously postulated that orgasmic sensation may occur through recently discovered genital taste bud-like structures. The interaction between the pudendal nerve and Onuf’s nucleus may be important for developing orgasmic information. The study aims to investigate whether ischemic damage to Onuf’s nucleus-pudendal network following spinal subarachnoid hemorrhage (SAH) causes taste bud degeneration or not.
Methods: The study was conducted on 22 fertile male rabbits who were divided into three groups: control (GI; n=5), SHAM (GII; n=5) and study (GIII; n=12). Isotonic solution, .7cm3, for the SHAM, and .7cm3 homologous blood was injected into spinal subarachnoid spaces at S2 level of the study group. Two weeks later, Onuf’s nucleus, pudendal ganglia and the taste bud-like structures of the penile urethra were examined histopathologically. Degenerated neu- ron densities of Onuf’s nucleus, pudendal ganglia and atrophic taste bud-like structures were estimated per mm3 and the results analyzed statistically.
Results: The mean degenerated neuron densities of taste bud-like structures, Onuf’s nucleus and pudendal ganglia were estimated as 2±1/mm3, 5±1/mm3,6±2/mm3 in GI; 12±4/mm3, 35±9/mm3, 188±31/mm3, in GII and 41±8/mm3, 215±37/mm3, 1321±78/mm3, in GIII. Spinal SAH induced neurodegeneration in Onuf’s nucleus, pudendal ganglia and taste bud atrophy was significantly different between GI/GII (p<.005); GII/GIII (p<.0005) and GI/GIII (p < .0001).
Conclusion: Ischemic neuronal degenerations of Onuf’s nucleus and pudendal ganglia following spinal SAH lead to genital taste bud-like structure atrophy. This mechanism may be respon- sible for sexual anhedonia and sterility in cases with spinal cord injury, which has not been documented so far. More studies are needed