How do vagal afferents contribute to genital sensation in people with spinal cord injury?
Executive summary
Vagal afferents can provide an alternate, spinal‑cord‑bypass route for genital sensory signals in people with spinal cord injury (SCI), especially documented for vaginal–cervical sensation in women via activation of brainstem centers consistent with vagal input [1][2]. The evidence combines human functional imaging, animal models showing vagal sprouting or expanded visceral innervation after decentralization, and physiological reviews that place the vagus alongside pelvic and pudendal pathways while also noting important limitations and unanswered mechanistic questions [3][4][5].
1. The direct imaging signal: fMRI evidence of a bypass pathway
Functional MRI studies of women with clinically complete suprasacral SCI showed activation of the nucleus tractus solitarii (NTS) and higher limbic and cortical sexual‑response regions during vaginal–cervical self‑stimulation and orgasm, findings the authors interpreted as strong evidence that vagal afferents transmit genital sensation directly to the brain without traversing the spinal cord [1][2].
2. How the vagus could carry genital signals: anatomy and plausible routes
Although classic textbooks emphasize pelvic, hypogastric and pudendal genitospinal afferents to the sacral cord, the vagus also carries visceral sensory fibers from pelvic organs and projects to the NTS in the medulla; these anatomical connections make it physiologically plausible that uterine/cervical/vaginal input can reach supraspinal centers via the vagus [5][3].
3. Animal experiments and plasticity after injury: sprouting and neurochemical change
Preclinical studies report vagal sprouting to pelvic targets — for example, vagal innervation of the clitoris and bladder in canine and rodent models after pelvic decentralization — and SCI‑associated neurochemical plasticity in nodose ganglion neurons that could alter vagal signaling post‑injury, suggesting compensatory reinnervation or sensitization might underlie some post‑SCI genital sensations [4][6][7].
4. Who experiences it and what is missing: population, sex differences, and methodological limits
Human reports document that a subset of people with clinically complete injuries (notably women with lesions above T10) retain perceptual awareness during genital stimulation, but sample sizes are small and “complete” by clinical criteria does not guarantee true anatomical transection; residual spinal fibers, alternative peripheral pathways, and individual variability mean the vagal explanation is compelling but not definitive for all cases [2][3][8].
5. Clinical and therapeutic implications, and competing explanations
If vagal pathways or post‑injury vagal plasticity contribute to retained genital sensation, this opens possibilities for neuromodulation and reconstructive strategies (for example dorsal genital nerve stimulation or surgical nerve transfers) to restore or enhance sexual function, yet clinical trials remain preliminary and other mechanisms — residual spinal transmission, somatic nerve rerouting, or central reorganization — remain viable alternative explanations that the literature explicitly acknowledges [9][10][11].
6. Bottom line and research priorities
The convergent evidence — human fMRI implicating the NTS, animal models showing vagal sprouting, and neurochemical changes in vagal afferents after SCI — supports a real role for vagal afferents in some cases of preserved genital sensation after SCI, but the phenomenon is incompletely characterized: larger human studies, careful anatomical verification of injury completeness, sex‑comparative work, and mechanistic experiments are needed before stating how often or by what exact molecular processes the vagus substitutes for genitospinal pathways [1][4][6][3].